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What is it about the housekeeping genes that makes them almost immune to gene regulation?
When it comes to eukaryotes, including ourselves, we have all different kinds of specialized cells and tissues that are so different, yet originally all came from the same single cell. And apparently the reason for that is differential gene expression, where different genes get to be expressed in different cells. But there are, however, a set of genes that gets to be expressed in almost all of the cells.
My question is not why, but what is it about these genes that in a way makes them above the laws of regulation? Is it in their sequence? Or are they located on a single chromosome or perhaps regions that are somehow non-regulatable?

Housekeeping genes aren't clustered on a single chromosome. It is perhaps not that 'housekeeping' genes - broadly expressed genes - are 'above the laws of regulation'; rather that their regulation is merely more straight-forward than that of specialised genes.
I can think of 2 factors that could be relevant:

Abundance of methylation sites (CpG sites)
Promoter sequences and hence the transcription factors regulating expression of housekeeping genes are distinct from those controlling specialisation

I think the second (promoter sequences) is the better explanation, since housekeeping genes are abundant in CpG islands; but I'll explain a bit about both.
tl;dr: Housekeeping genes have simpler promoter and enhancer regions that are not bound by particular complexes which act to inactivate regions of the genome in a hierarchical manner during differentiation (according to the transcriptional program). http://genomebiology.com/2007/8/7/R140
Preamble
In forming tissues during development, cells must differentiate from embryonic stem cells, which have very wide potential to express many genes and give rise to all cell types; to partially specialised stem cells e.g. hematopoietic stem cells (HSCs) which are limited to give rise to all blood cells but not, say, neurons or pancreas or skin. Completely differentiated cells have a much more restricted domain of possible expression, and are more-or-less condemned to their fate.
Waddington's developmental landscape is a nice metaphor for how cells specialise:

DNA Methylation
A major mechanism behind this one-way narrowing of potential is methylation of DNA, which suppresses transcription. As the ball rolls down the landscape it acquires new stretches of methylation on its DNA, rendering it inactive which (for our purposes) is permanent and irreversible.
DNA methylation consolidates its chromatin inactivating function by acting as a signal for proteins which chemically modify histones (around which DNA is wrapped in chromatin) with further signals to condense chromatin, which occludes the transcriptional machinery from doing what it does best. (There are also activating histone modifications, and we imagine chromatin being, roughly, in OPEN and CLOSED states regarding the possibility of RNA polymerase gaining access to the DNA.) Since histones are ubiquitous & regularly spaced over the genome, there aren't "non-regulatable" regions - chromatin is opened or closed by the interactions of various DNA binding proteins, some reading and writing signals on to the chromatin.
So one plausible hypothesis is that housekeeping genes are relatively devoid of CpG sites (where methylation occurs). However I think this is not true. Many human genes have regions abundant in CpG (called 'islands') around their promoters, and in particular virtually all housekeeping genes. When genes are active, these CpG islands are unmethylated - hence in most tissues housekeeping genes have unmethylated CpG islands, something else is keeping them unmethylated.
Specialised cells, through a hierarchical transcriptional program of 'master regulators', successively close unneeded regions of their chromatin during differentiation, and keep open regions containing housekeeping genes, and the 'specialised genes' that relate to its specialism - these regulators are transcription factors which recognise the regions they act upon by binding promotor or enhancer sequences.
Housekeeping promoters and transcription factors
Transcription factors bind to enhancer or promoter sequences and open or close the chromatin for RNA polymerase, usually as part of a co-operative complex of many factors, including proteins that modify the histones or methylate DNA.
A good hypothesis is that the promoter/enhancer regions of housekeeping genes differ from those of specialised genes which are inactivated in many tissues. The transcriptional programs in differentiation must call forth factors that bind and inactivate specialised genes but keep active things like actin, ribosomal genes, etc.
This paper finds that upstream regions of housekeeping genes are less conserved, and a particular set of promoter motifs are over-represented. This suggests that housekeeping genes have relatively simple regulation by a few transcription factors; they lack binding sites for those transcription factors with important specialised roles in development.
To summarise, I think the following is likely: Housekeeping genes' promoter and enhancer regions exempt them from the complex transcriptional programs of hierarchical inactivation responsible for cell differentiation that many other genes are subject to. Housekeeping genes simply lack the relevant binding sites for these specialised transcription factors; they have instead more simple 'core' promoter elements. All the DNA methylation and opening/closing of the chromatin is a consequence of the transcriptional program.

http://en.wikipedia.org/wiki/CpG_site
http://en.wikipedia.org/wiki/Embryonic_stem_cell
http://en.wikipedia.org/wiki/Hematopoietic_stem_cell
http://www.nature.com/scitable/topicpage/the-role-of-methylation-in-gene-expression-1070
http://en.wikipedia.org/wiki/Histone
http://genesdev.cshlp.org/content/25/10/1010.full
http://genomebiology.com/2007/8/7/R140   < most relevant thing to read, and the basis of my own conclusion

The problem with housekeeping genes is that they are often not stable and their expression depends on the cell types as well as the conditions. They can be stable under one condition, but are not under another. So this needs to be tested every time you have to choose a housekeeping gene - always use GAPDH or beta-Actin simply doesn't work or skews the results.
The reasons why the housekeeping genes are chosen is because they are thought to be independently expressed (more or less) in the cells and that the actual experiment has in influence on them. This is also the reason why genes involved in the energy metabolism or the structural integrity of the cell (like GAPDH or beta-Actin) are chosen. This idea is not wrong, but needs to be tested, since transcription regulation networks are complicated and often bear interesting, surprisinf (and unknown) relations.
The following articles should be interesting in this context:

Reference Gene Validation Software for Improved Normalization
Selection of suitable housekeeping genes for expression analysis in
glioblastoma using quantitative RT-PCR
Reference genes in real-time PCR

What also gives quite a lot of information including a large number of references on this topic is the website from Gene Quantification (which sell products in this field).

Great answer - common misconception that "house keeping genes" are consistent in expression when used as reference genes. It is common practise to include several reference genes in many experiments and to confirm empirically that they do not vary between your samples.

Either this - or (what I have also done) is to test a number of genes and then choose the stable ones.


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How to engineer chromosomal duplications?
Specific genetic engineering of chromosomal aberrations like deletions, inversions and translocations are doable by using the CRISPR/Cas system or the other programmable nuclease systems. Insertions are also possible but mostly limited by the size of the insert.
Here two papers on the topic:
http://www.nature.com/nrg/journal/v15/n5/full/nrg3686.html
http://www.nature.com/ncomms/2014/140424/ncomms4728/full/ncomms4728.html
However these methods appear to be inadequate in case you want to insert a long DNA piece (>1Mb) into a chromosome (in case you want to engineer a duplication).
As far I have understood, problems arise when 1) you want to make such long DNA in the first place and 2) --suppose you have the DNA-- you need to transfect it into the cell...
Does anyone know how to tackle the genetic engineering of a large  chromosomal duplications? Is there any way to induce it without the need of supplementing the extra DNA?

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Are there U-rich transcriptional pause sites?
I've heard a statement in a talk that U-rich sequences cause transcriptional pausing. The intuitive explanation for this was that the UTP concentration is lower in the cell than the ATP concentration. Reducing the concentration of an educt obviously reduces the reaction rate, leading to pausing of the RNA polymerase.
After reading up on transcriptional pausing, I haven't found any literature that shares this view. The recent papers I found don't show U-rich sequences and have completely different explanations on how pausing works. Those explanations mainly concern interactions at the edges of the transcription bubble.
Now, I guess that there might be multiple mechanisms of transcriptional pausing. But I couldn't find any references in the literature to U-rich pause sites and how they could work. Is there any literature on this? Either on the fact that U-rich sequences tend to be pause sites, or that the concentration difference in NTPs leads to pausing at certain sites.

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I am not sure about polyU's effect on transcription rate but I don't think UTP is ever in limiting concentrations. Poly-pyrimidine tracts (PPT) are present near splice sites and this paper suggests that PPT-binding protein (PTB) can affect the rate of polyadenylation. I am not sure if that is what you are interested in

Yes, there are: this is a feature of bacterial intrinsic termination. The mechanism of pausing is not as you describe, though.
In bacterial transcription, two forms of termination are recognised (to my knowledge):

Intrinsic termination, consisting of a hairpin and a stretch of Uridines.
Rho-dependent termination, consisting of a 'loading' site for termination protein Rho, and a pausing site, but not the stretch of Uridines you refer to.

If you were reading up on transcription in eukaryotes, or were reading about rho-dependent termination, that would explain why you found no mention of polyU tracts. When evolution provides many solutions to a problem, it can get tricky to keep on top of it all!
This lists a few types of termination, including attenuation which is fascinating, and does involve regulation dependent on the concentration of a substrate.
Intrinsic Termination
A palindromic sequence situated just before the termination site causes a hairpin to form in the nascent RNA inside the exit channel of RNA polymerase, if given time (and if anti-termination factors do not bind the RNA to suppress hairpin formation). It appears that formation of this hairpin "destabilises the elongation complex [RNA polymerase + elongation factors]", and is an irreversible step towards collapse of the transcription bubble and dissociation of the transcription machinery.
The polyU tract (~8nt long) proceeding the hairpin seems to have dual function: the A:U basepairing in the DNA:RNA hybrid is weak; the hybrid becomes less favourable. Since the hairpin (which is an RNA:RNA duplex) is adjacent to the RNA:DNA hybrid duplex in the bubble, they experience competition for formation. Weakening the hybrid duplex favours hairpin formation, which acts like a switch that separates most of the RNA:DNA duplex in the bubble - synthesis cannot proceed, and the unstable complex dissociates.
Also, the ployU seems to be responsible for pausing which allows time for the hairpin to form, but not for the reason you suggest:
The concentration of UTP in the cell is not unusually low. ATP concentrations are higher than other ribonucleotides since it is the cell's major 'energy currency', quite apart from nucleic acid synthesis. Hence I don't believe pausing can be explained as the polymerase waiting for UTP. The polyU tract probably acts as a 'back-tracking signal' to the polymerase, since the hybrid duplex in the catalytic site is weakened, and the repeated nature may be "slippery"(?). This back-tracking pauses the polymerase.

To summarise: The elongation complex passes the palindrome and reaches the polyU tract, where the hybrid duplex in the bubble is weak and tends to cause back-tracking/pausing. This allows time for the hairpin to form in the exit channel, which both unwinds the hybrid duplex further, and destabilises the elongation complex. The transcriptional machinery is now destined to dissociate and the bubble collapse: RNA is released from the DNA duplex.
It is interesting to note that intrinsic termination can be suppressed by proteins that bind the hairpin. In bacterial operons, where sets of (almost) concatenated genes are separated by intrinsic termination signals, the amount of read-through at each termination site determines the relative expression levels of each gene.
Rho-dependent Termination
Rho is a hexameric protein complex that is loaded on to the nascent RNA at a loading sequence. It hydrolyses ATP to move along the emerging RNA - apparently it "races" with the polymerase, and when it catches up to the polymerase, it causes termination. There are pause sites in the RNA which allow rho to catch up - these sites tend to be rich in A and U, so perhaps polymerase is slowed by destabilisation of the hybrid duplex - but it is nothing like the intrinsic terminator, since it depends completely on rho for termination.

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Why aren't circadian rhythms exactly 24 hours long?
Most organisms exhibit circadian rhythms that have a periodicity of about, but not exactly 24 hours. Why is this? And to what extent can variation in periodicity in circadian rhythms among the individuals of the same species (if a variation does indeed exist) influence the level of competition they face in acquiring resources?

Regarding the first question, probably because as long as the organism uses queues from it's environment (e.g. light levels / temperature / tides) it's rhythm doesn't need to be exactly 24 hours. It just has to be good enough, and the organism will use these queues to adjustment its behavior accordingly. Regarding the second question, it should probably be split off into a different question.

When you ask “why,” are you interested in the molecular mechanism of this variation or the adaptive “reasons” behind it? The title question is more intuitively the former to me, but the second sentence in the body of the question points more toward the latter. If both, I agree with the prior commenter that two separate questions may be in order. @p.s.w.g: indeed, Zeitgebers.

Can you add a couple of references for your claim that "circadian rhythms that have a periodicity of about, but not exactly 24 hours" (will also show the taxonomic scope)?

@Susan and I am interested in the adaptive reasons and the evolutionary significance behind my questions. I found one answer to my first question - that if all individuals of a population had the exact same periodicity, then they would have to face more competition in acquiring resources (I found this on surfing the net). I wasn't entirely convinced, and hence my second question. Sorry for not making the connectivity clear.

Perhaps because the optimal cycle of life is not 24 hours due to seasonal changes and migrations? It is quite difficult to make biological oscillators with very long periods precise, and it doesn't need to be, because one can entrain an oscillator with external stimuli. And as you mentioned in the comments, variations can be helpful in many ways.

I think the notion of 23 hours comes from sleep experiments. No ref, sorry.

Biological/organic systems are notorious for imprecision, making a perfect 24-hour cycle practically impossible - nevermind the fact that "hours" are a purely artificial concept that humans invented to help make sense of time.
The simplest "close-enough" way to measure days that doesn't require an implanted clock microchip or heavy computing power is to detect extreme changes in light or temperature associated with transition between day and night.
An extra argument against hard-locking to a 24-hour cycle: Adaptability and migration. If every life form is locked to a strict 24-hour cycle with fixed time slots for sunset and sunrise, this limits migratory adaptation since different regions have different sunset/sunrise and day lengths at different times of the year. Timing a wake-up and sunrise and sleep at sunset (or the reverse among nocturnal species) generally works across most of the planet no matter the season (the only exception being the niche case of a solstice at the poles, for example http://www.slate.com/blogs/bad_astronomy/2016/06/22/why_does_the_sun_never_set_at_the_north_pole_in_the_summer.html )
There's also some evidence that days on Earth are getting longer ( see
https://www.space.com/40802-earth-days-longer-moon-movement.html )

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How can heart disease cause dizziness after eating?
I have been reading several articles explaining dizziness after eating (see here and here), and both articles gloss over something that I found pretty remarkable.
Both articles claim that "heart disease" can cause one to experience dizziness after eating. For instance, as one article merely generalizes:

A healthy heart is needed to pump blood faster during digestion. Certain heart conditions can lead to its inability to send enough blood to the abdominal organs, which may lead to a drop in blood pressure, resulting in dizziness and sometimes, nausea.

To me, this is pretty vague and uninformative. Making a blanket statement like "certain heart conditions can...lead to a drop in blood pressure" is like saying "not eating or drinking water can cause death."
I'm interested in are the hows and the whats: How does/can heart disease cause dizziness after eating, what are the reasons why this happens, and what are some examples of heart disease ("certain conditions") that cause this (as I'm sure there are many similarly-related diseases)?

Dizziness after eating, which can lead to falls and passing out, is called postprandial hypotension, and as the heart is indeed responsible for responding to hypotension by increasing it's rate - which can be seen in any number of clinical scenarios from blood loss to standing up too suddenly - failure to do so, for any reason including heart disease, can result in continued hypotension, which is experienced by most of us as dizziness.
Postprandial hypotension (PhTN) is defined as a fall in systolic blood pressure (SBP) of ≥ 20 mmHg occurring within 2 hours of a meal. This hypotension (hTN) can result not only in dizziness, but  may also cause syncope, falls, weakness, angina pectoris, and stroke.
Because PhTN is particularly common in older hypertensive patients, and older patients tend to have higher incidences of heart disease, it was initially thought heart disease was the cause. However, that didn't explain why some young people without heart disease have PhTN.
In truth, the mechanism of PhTN is not fully understood.
Normally after a meal, blood supply to the gastrointestinal (GI) tract increases, starting with increased flow through the left gastric and celiac arteries, followed by the mesenteric artery, which is more prolonged. Observations indicate that the postprandial hyperemia progresses along the GI tract in association with the movement of ingested food. The magnitude (25–200%) and the duration (3–7 h) of the hyperemia appear to depend somewhat on the composition of the meal. The increase in GI blood flow means there's less blood to circulate in the rest of the body (relative hTN). Normally this is corrected for in various ways.
Baroreceptors (nerve cells within arteries near the heart and in the kidney) are sensitive to rises, falls, and the rates of change in BP, but are especially sensitive to sudden falls in BP, which results in decreased baroreceptor firing. Autonomic Nervous System responds by increasing sympathetic outflow and decreasing parasympathetic (vagal) outflow. Sympathetic outflow leads to vasoconstriction (increased systemic vascular resistance, or SVR), increased HR (tachycardia) and increased force of contraction on the heart (positive inotropy). This leads to a partial restoration of arterial pressure. In people with PhTN, any abnormality at any point in the system will result in an insufficient rise in SBP to overcome the fall.
Therefore possible contributors to PhTN include inadequate sympathetic nervous system compensation for meal-induced GI blood pooling; impairments in baroreflex function; inadequate postprandial increases in cardiac output; impaired peripheral vasoconstriction, as well as abnormal responses to GI hormones released during digestion.

Dysautonomic patients with postprandial hypotension fail to maintain systemic vascular resistance after a meal. This impairment in vascular response to meal ingestion may underlie the development of PhTN. Power spectral analysis suggests an impairment in the postprandial autonomic modulation of HR in healthy elderly and dysautonomic subjects, possibly predisposing to hTN when vascular compensation is inadequate.

Heart conditions that might result in an inadequate response to PhTN include low heart rate (bradycardia), heart valve problems (decreases cardiac output), heart failure (decreased ejection fraction equals cardiac output), patients with atrial fibrillation (decreases cardiac output because of inadequate filling of ventricles), heart attack (decreased ejection fraction), heart muscle disease (cardiomyopathy), severe left ventricular hypertrophy, people with HTN on medications which cause a lowered heart rate, etc.
Therefore, Postprandial Hypotension is an important hemodynamic abnormality in patients with cardiac diseases as well as autonomic nervous system abnormalities such as can be seen in Parkinson's Disease, diabetes mellitus, and others.
Postprandial Hypotension: Epidemiology, Pathophysiology, and Clinical Management
Association of postprandial hypotension with incidence of falls, syncope, coronary events, stroke, and total mortality at 29-month follow-up in 499 older nursing home residents.
Postprandial hypotension. Pathophysiological mechanisms and clinical implications in different disorders.
Postprandial hypotension in response to duodenal glucose delivery in healthy older subjects
Postprandial Hyperemia
Arterial Baroreceptors

Vasoconstriction from sympathetic outflow is not generalized. It causes selective vasoconstriction, where skeletal muscles are excluded. I believe the viscera are also spared as sympathetic activation of viscera would inhibit digestion itself? Can you please clarify @anongoodnurse?

What I am asking is if sympathetic system will cause only peripheral vasoconstriction and not general vasoconstriction? Very nice answer BTW...

@CRags - the effect of sympathetic output is complex, involving not only norepinephrine acting on alpha receptors, but epinephrine, angiotensin II and vasopressin, among other vasoconstrictors. And, no, it does not have the same effect everywhere. The question was not about the sympathetic nervous system, but about PhTN. It's long enough! ;)


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Why is it that heterozygous loci appear as two separate bands during gel electrophoresis while homozygous loci appear as one band?
Is it because heterozygotes have a greater base pair length? (And if they do, why is that?) Or is it because recessive alleles are moving slower than the dominant alleles in the gel?

If a loci is heterozygous there are two different alleles coding for the same Protein. The alleles may differ in their lengths. With a gel electrophoreses you split DNA fragments by their length.
Homozygous -> same alleles -> same length -> one band. | Heterozygous -> different alleles -> different length -> two bands
Is this what your question was about?

Your question is the answer. Hetero = different, thus you have two different bands, representing two versions/alleles of one gene. Homo = equal, thus you only have one version of a gene. These alleles may differ in length and/or restriction sites, resulting in different bands, because electrophoresis is based on molecular weights.

It depends what molecule you are running on the gel and how it was treated beforehand. Are you referring to restriction fragment length polymorphisms of DNA, or another type of assay? You need to understand the method to understand the result!

@WYSIWYG - I think your answer is pretty interesting and I like this question. Could you not convert it into a [short?] answer? My +1 is for you already :) All this closing of questions... sometimes a good answer may actually emphasize the strengths of an apparently weak question! I vote for leaving open.

Okay @ChrisStronks, boss is away today and no work pending. So passing time by digging old unanswered questions :) Will post it as an answer.

@WYSIWYG : sounds good! i just saw that there is already an answer that includes your argument. This may save you some work :)

@WYSIWYG - Nice answer, especially with the resolving power of gels included. +1!

@ChrisStronks Thanks. I had tried to answer some other old questions. Please have a look at them and let me know if anything else is needed. The answered question had gone down by 1% : so all this effort :P

Let us continue this discussion in chat.

A heterozygous locus has two different alleles and therefore it is possible that their DNA sequence lengths are different. However, it is unlikely that they are so different so as to be clearly resolved in a gel electrophoresis. Agarose gels can at best resolve 20bp; polyacrylamide gels can resolve smaller differences but it is only done for small DNA fragments.
I think upto 50bp difference is possible between alleles. But such huge insertions/deletions are rare and the difference between the alleles is usually a point mutation or small insertions/deletions(indels). Big indels are possible when a transgene is inserted specifically in one chromosome; these cases are mostly experimental.
If you consider paralogs as alleles then they can be of different lengths and can be resolved in agarose gels— usually the difference is in the untranslated regions. If you are doing Southern blot and using a probe that can bind to both paralogs then you will end up getting two bands.
Having said that, it is possible to see a difference in gel bands even if there is no size difference. This is possible by a technique called RFLP. In this technique the DNA is digested using a restriction enzyme which basically cuts the DNA at a specific sequence (usually a hexamer). If a point mutation abolishes or creates a restriction site then the fragment length would be different between the alleles. This is detectable on the gel.
A similar technique is AFLP.

the restriction enzyme analyses are an interesting addition for sure

Heterozygous loci have both alleles present at a given time, for example Aa (considering diploid organism), where as homozygous have only one type (AA or aa). Generally, both alleles have different sequence lengths due to deletions, insertions etc. so if any locus is homozygous, it will produce only one length but heterozygous will produce two different lengths. That is why you will only see one band in case of homozygous and two in heterozygous.

Why would AA, Aa, and aa produce different lengths if they each contain two alleles? Shouldn't they each project two different bands on the gel?

Only Aa would produce two bands but AA and aa would produce only one band. Imagine, for example, allele 'A' has length 100bp, allele 'a' has length 95bp. So if an individual is only AA, it will produce two bands, one for each A and A but since both of them are same length, they will overlap and appear as only one band on gel. Similar is the case for 'aa' individual. However, when Aa individual produce two bands they differ in length, so it will produce one band at 100bp and one at 95bp. Hope this helps.


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Average dimensions of the human back (anthropometry)
I am wondering if anyone can point me to (a scientific source that provides) the estimates of the dimensions (length x width) of the human back?
I am specifically interested in the dimensions (length * width, or surface) of the lower back of the average adult, and in specific the region between the 7th thoracic and 4th lumbar vertebra - i.e., the region between T7 - L4 in the image below:
Ideally a distinction is made between males and females and perhaps kids as well. The area of research dealing with this matter is anthropometry.

Please mention the source to any information provided. I have access to some not-scientifically based sources (clothing companies for example). Although additional such sources are welcomed, scientifically-based answers are preferred.

Although not very related, this set of drawings is very interesting: http://www.jneuhaus.com/human.html

http://brml.technion.ac.il/publications_files/1195633781.pdf

Here they give the dimensions of the entire back, if that interests you: http://msis.jsc.nasa.gov/sections/section03.htm#_3.3_ANTHROPOMETRIC_AND

This doesn't really answer the question and I only post it at the asker's request.
NASA has measured the dimensions of the back in 40 year old American males and 40 year old Japanese females in the year 2000 at 1G. Of course gravity matters to NASA…

From figure 3.3.1.3-1 (American male). All data in centimetres:

921 Waist back

5th percentile: 43.7
50th percentile: 47.6
95th percentile: 51.6

506 Interscye

5th percentile: 32.9
50th percentile: 39.2
95th percentile: 45.4


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How to decide if genes are linked in an unordered mapping problem?
From what I understand, if the tetrads resulting from a cross exhibit the same number of parental ditypes as there are nonparental ditypes, then the genes under consideration are said to be unlinked.
For example, say I cross two gametes containing $ab^+$ and $a^+b$, respectively, and get 170 tetrads exhibiting parental ditype (all offspring are $ab^+$ or $a^+b$), 165 exhibiting nonparental ditype (offspring are $a^+b^+$ or $ab$), and 30 exhibiting tetratype (offspring one of $a^+b^+$, $a^+b$, $ab^+$ or $ab$).
I'm not sure whether to classify these genes as linked or unlinked. I want to say yes, they are indeed linked, but 170 and 165 seem like close enough numbers to suggest they may be unlinked.
I would think the ratio of parental to nonparental ditype has to be considered close enough to 1, but how do we decide a threshold for that?

I'd use a chi-squared test.  You calculate what you expect to see if your hypothesis is true, and you take what you do see, and the chi-squared result tells you how likely it is that your results are different enough from what's expected to indicate that your hypothesis is incorrect.

Okay that makes sense to me. Is there a way to know the expected distribution for the tetrad genotypes?


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Why is the resting potential of a neuron so close to the equilibrium potential of K⁺?
I know this has something to do with the K+ leak channel. I just don't understand how.
I know that 3 Na+ are pumped out for every 2 K+ pumped in. This makes the cell interior net negative.
I know that K+ is allowed to leak out slowly via K+ leak channels.
How does this place the resting potential of the cell so much closer to the equilibrium potential of K+ than Na+?

Lets just go with the basic Hodgkin-Huxley equation:
$$C_M \frac{\text{d}V}{\text{d}t}=-g_{Na}(V-E_{Na}) -g_K(V-E_K) -g_L(V-E_L)$$
At rest ${\large\frac{\text{d}V}{\text{d}t}}=0$ and therefore $V$ is dependent on the conductances ($g_X$) of different ions. Since $g_K \sim 30\times g_{Na}$, the resting potential is closer to $E_K$ (Nernst equilibrium potential of K+).
What it basically means is that since potassium has higher membrane conductance, it diffuses faster thereby attaining equilibrium faster than sodium (in isolated cases assuming only one ion at a time). When both ions are present the resting potential is because of both the ions but since K+ diffuses faster, it has a major contribution to the resting potential compared to Na+. Leak current that is described in the above equation is a general leak (non-specific). Other channels like rectifiers and voltage gated channels are important when talking about action potential and all these channels contribute to the conductance; however you can group all that into a single metric called membrane conductance. Voltage gated channels can be considered separately when studying the dynamics (in this case the conductances themselves become a function of voltage).

Well, thank you. However, could I ask for a slightly less technical answer? Basically the potassium ions are 30x more conductive, so they have greater determining power over what the resting potential is? So K+ leak channels don't really have anything to do with resting potential.


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What is topological crossover?
I read about "topological crossover" in this paper, Table 1. What does this refer to?

The link is currently dead. Can you add a full reference, explain what the article is about and exactly how you find it unclear.

@fileunderwater - The link is functional

@ChrisStronks Not for me: "Error: Sorry, your request can't be processed due to a system problem.". Questions must be more self-contained either way, and not depend on a single link to be understandable.

ScienceDirect has accessibility issues lately. The table is rather large and the captions totally uninformative. I scanned the article link and I really dunno what topological crossovers are. It seems to be some sort of aminoacid inverted tandem repeats. I think it's an interesting question actually.

The DOI is doi:10.1016/j.ijmm.2014.12.010. For those with access issues (it's an open-access article), I put a PDF in my Dropbox here.

You may not want to know. It really depends on how good your math background is.

A topological crossover is a class of representation independent operators that are well defined once a notion of distance over the solution space is defined [1].

Let's first start with the definition of Topology.

Topology is the mathematical study of shapes and topological spaces. It is an area of mathematics concerned with the properties of space that are preserved under continuous deformations including stretching and bending, but not tearing or gluing. This includes such properties as connectedness, continuity and boundary [2].

Later on in the paper they start to mention transverse topology which leads to Differential Geometry.

In mathematics, transversality is a notion that describes how spaces can intersect; transversality can be seen as the "opposite" of tangency, and plays a role in general position. It formalizes the idea of a generic intersection in differential topology. It is defined by considering the linearizations of the intersecting spaces at the points of intersection [3].

To understand the underlining math concepts of this paper, you may need a rigorous background in mathematics. I would check the authors backgrounds to see if they are Physicists or Mathematicians.
Most students in mathematics generally take two courses in introductory real analysis and at least one course in abstract algebra before taking topology. The standard book for a first course in topology is by Munkres.
A book you may want to look into is Topology in Molecular Biology. However, the author is a mathematician, so if you are not, you may need to start with courses in analysis, topology, differential geometry before you tackle this book. I have never seen the book so I don't know how difficult it will be but here is the about the author from amazon:

M.Monastyrsky is a professor of mathematics and theoretical physics
  at the Institute of Theoretical and Experimental Physics, Moscow, Russia,
  graduated the mathematical department of Moscow state university(1967),
  author of numerous papers in diferent fields of mathematics and
  theoretical physics including the monograph :Topology in Gauge Fields
  and Condensed Matter (Plenum,1993 ) and two other books:Riemann,Topology
  Physics, Birkhauser, Boston, 1999, 2nd ed. and Modern mathematics in the
  light of Fields medals, AKPeters, 1997.I gave invited plenary talks on
  many conferences and was the visiting professor of many universities
  and institutes including IAS(Princeton), Harvard, Princeton and Yale
  Universities (USA), Cambridge and Oxford Universities (Great Britain),
  IHES and Universite de Paris (France).

Helpful answer. Seems I would have to invest some time trying to understand this.


text:
Why do eyes water in response to particular emotions?
It is common for people to experience very moving situations (sad movies, etc) and have a physical reaction to it (such as crying). I am curious about how emotions can physically lead to the act of crying. Why/how does this happen? What is the mechanism?

Can you please clarify this question, and also support your assertion with a little bit of the background reading you've done about it?

@anongoodnurse Many questions about biology are so obvious from the human perspective, that no reading should be asked.

When we are sad, our emotions are in an overdrive and the parasympathetic nervous system triggers lacrimation i.e. tears, and we cry.

Great succinct answer for a vague topic.

You're only answering the proximal (physiologic) why, i.e. the mechanism. What about the distal (evolutionary) why?


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What's the difference between stabilizing selection and balancing selection?
I came across these terms in Darwin's "Origin of Species" and I wasn't sure what the difference is.

Usual meaning
Usually, Stabilizing selection is a concept that applies to a phenotypic trait while balancing selection is a concept that applies to a given locus.
Balancing selection can either be due to negative-frequency dependence selection or due to overdominance (=heterozygous advantage at a single locus).
What Darwin may have meant
Because Darwin didn't know about genes, he was necessarily not using the term balancing selection as I am using it. I can think of several more or less related pattern of selection that might fall withing the definitions for "stabilizing selection" and/or "balancing selection". Maybe he meant "frequency-dependent selection", "positive selection for an intermediate trait", "varying selection through time (temporally heterogenous environment)" and "varying selection through space (spatially heterogenous environment)". Eventually again, that might mean "positively correlated traits that undergo opposite selection pressure (or the opposite)" but that would definitely be surprising.

I think the key distinction here is that stabilizing selection promotes a monomorphic population whereas balancing selection preserves polymorphism.


text:
Is using Hidden Markov Models to find homologues sensible in abstract, short sequences?
HMM alignment tools like hhpred excel at finding subtle homologues of folded proteins that simpler scoring techniques (such those used in BLAST algorithms) would miss.
I am only looking at a small (20AA) sequence and it is helical throughout.
Is hhpred still likely to pick up on subtle similarities in the basic secondary structure as it would in a folded protein sequence, or would simpler alignment be just as appropriate?

Hi there - seems like you may get an answer from someone on BioStars or another site with more computational/statistical expertise - as this question is not really biological per se, more bioinformatic

Thanks for the tip, I'll give that a go. I think this question is right at the fringe of what is appropriate for this site, but you never know! Someone might have come across this problem before!

TMHMM is a very good standard on predicting the TMHs in the first place, so it stands to reason that predicting homologues using this approach is completely viable.


text:
Why do human eyes glow red on a photo and dog's eyes green?
Previous Research
I know that cameras sometimes come with an anti "red eye" functionality that involves two flashes, presumably the second flash coincides with the shutter opening.
Question
Why do camera flashes sometimes lead to photos of humans with red eyes? And why do dog's eyes appear green?
Related
The reason for the green dog's eyes has been answered quite shortly under the question "why-do-dogs-eyes-glow-green-on-a-photo", but that question does not answer my specific question: Why do humans have red eyes on flashed photos and why are dog's eyes  green?

It's considered a requisite on biology.se that at least some sharing of your reading/research is presented with your question. Why do you think the retina is red? Otherwise it will be closed. The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here.

I have edited the question to emphasize the difference between the dog's green-eye effect in the linked question and the human's red eyes. The answer still talks a lot about the human situation, which was the original question

@anongoodnurse let me know if my edit is sufficient background

@ChrisStronks TQ I did notice the dog question had a very weak implication of an answer to this question, but felt the human version deserved its own thorough answer

@hello_there_andy - I totally agree with both your remarks. The other answer was kind of vague, and the human red-eye was never asked before on Bio.SE as far as I am aware. The combination of both in one question makes it a nice new question definitely deserving to be asked! Hope my answer helped.

Short answer
In humans it is basically the red choroid plexus in the back of the eye you are seeing on a flashed photo, while it is the green-reflecting tapetum lucidum in dogs.
Background
The red-eye effect in humans was explained nicely by Yale Scientific Magazine, and I adapted the following text from that source:
The human eye can effectively adjust to different light conditions, but this adaptation is also what leads to the red-eye effect. The eye regulates the amount of entering light by contracting or expanding the pupil. At night, your pupils will accordingly enlarge to extract more light from their surroundings. However, this dilation also leaves your eyes unprepared for the sudden burst of light from a camera flash.
When light from the flash enters your eyes under these conditions, your pupils are unable to contract fast enough (full constriction takes a few seconds) to prevent the light from reflecting back, off of the red blood vessels of the choroid. The choroid plexus nourishes the retina, and therefore contains ample blood supply. As a result, the camera will pick up the red reflection, resulting in the red-eye effect. Interestingly, due to their increased “dark adaptation,” children more commonly have red eyes in photographs.
The amount of melanin, a light-absorbing pigment in the eye, also has a role in the red-eye effect. Individuals with lower levels of melanin will absorb less and thus reflect more light, explaining the high incidence of the red-eye effect in albinos.
Though the cause of this effect is wired in the biology of the eye, some cameras can reduce red-eye by sending a few preliminary flashes before the final flash to give the pupils enough time to contract and adapt to the increased-light conditions. Another way to reduce the effect is to avoid looking directly into the camera lens, which will reduce the reflection of light. Finally, if all else fails, modern image editing software, such as Photoshop, can remove the red discoloration.
With regard to why dogs and other animals may not have red-eyes but other colors, this was indeed answered in your linked question: some animal species have a tapetum lucidum, which is situated in front of the choroid and reflects light back onto the retina thereby increasing light sensitivity. In dogs it is green, as aptly shown in the linked question's answer. The following figure shows the anatomy and the position of the tapetum in front of the choroid. It was adapted from Pets.SE with the related question "Should I be concerned that my dog's right eye is reflecting green in the dark when his left eye doesn't?"

Hence, the reason why animals with a tapetum lucidum have another eye color is that light does not reach the choroid in these species, giving rise to green-eye effects in dogs and cats (picture taken from Ask Nature):

worth noting not all dogs have tapetum, some breeds have lost them, they also have red eyes on photos.


text:
Is fever a disease or not?
I have seen this question where the author is asking why people take drugs for fever. So my question is: Is fever is a disease or not?

Fever is due to increase in the levels of some cytokines (IL 1 - being most common cause) in the body. These cytokines generally (speaking broadly) are secreted by either immune cells or injured cells. So when there is a large scale immune response or injury, the response is Fever. So Fever is a symptom showing what is happening inside the body

I know pretty much nothing in medicine!
Fever is an abnormally high body temperature. Fever is a symptom and not a disease per se. Different medical conditions (incl. various infectious diseases) causes a patient to have fever.
Note that fever might be in some/most situations an adaptive response to a disease. In other words, for infectious disease causing fever, fever might be good for the host and not for the parasite. However this issue remains controversial (see the post linked in the OP's question for more info).
As GoodGravy said in the comments, many people get confused and consider fever as a disease instead of what it really is; a symptom. One likely reason for this confusion is that when one has fever, (s)he very often treat fever directly (taking drugs like Aspirin for example) rather than treating the underlying cause (the virus for example) of the fever.

I agree, but furthermore to end the confusion: Fever is the symptom of an underlying disease/infection, but it is very treatable and often is treated rather than the underlying cause of the fever. I think the fact that the fever is treated rather than the infection is what causes confusion. Although if you were to be pedantic I suppose you are not in an eased state due to the fever so I guess semantically you are in "dis-ease" directly because of the fever... Let me think a while...

Any malfunctioning in the body is the result of either external pathogens, environmental changes or it can be manifested by the body itself. Based on which we can call it a disease or a disorder.
Some can be viewed with the help of its underlying symptoms. Fever is a natural response of the human body to any kind of imbalance, for example, temperature fluctuations, infections, etc., and that is why we can get fever by any number of reasons. What is important is that it shows us of some other underlying reason of change. Therefore I think it's more of a symptom than a disease.


text:
Why is cancer not a communicable disease?
I read another question where the author is asking about the infectivity of viruses. In the same vein, I am curious why cancer is not a communicable disease.

A cancer is not a pathogen
Cancer is a group of cells that (because of several specific mutations) start to duplicate abnormally. This group of cancerous cells are the own cells of the sick patient. It is not another species infecting the individual carrying the disease. It is the individual itself who developed the disease. Cancer is not a pathogen (but see below) that infect hosts and get transmitted from one host to another. It is more correct to picture cancer as an internal mistake of the body rather than as an external attack on our body. You might want to have a look to the wiki page for cancer for more information.
Transmissible agents that can cause cancer
Some cancers are caused by transmissible agents, such as oncoviruses. the transmissible agent may jump from one host to another and cause cancers giving the sensation that cancer is transmitted. It is just a sensation of course because in reality only the oncovirus gets transmitted and not cancer itself jumping from one host to another.
Cancers that become transmissible
Note however that it is not impossible to imagine a tumour jumping from one individual to another in cases where the immune response cannot detect cancer as 'non-self'. Some cancers are transmissible. Those cancers are called clonally transmissible cancer (As indicated by C Rags in the comments). Here is the list:

The Devil Facial Tumor Disease which occurs in Tasmanian Devils
The canine transmissible venereal tumour (article from Chris Stronks in the comments)
The Contagious reticulum cell sarcoma occurring in the hamster.

CTVT in  canines is transmissable : http://www.sciencedirect.com/science/article/pii/S0092867406009123

Please leave a comment when downvoting.

There are a total of 3 transmissible cancers in animals identified to date. One in Tasmanian Devils, another in canines, another in hamsters:http://en.wikipedia.org/wiki/Clonally_transmissible_cancer Good answer +1

I’m unhappy with this answer, and although I haven’t downvoted it, let me try explaining why it was downvoted. First of all, as you note yourself later on, your initial sentence is simply wrong: many cancers are caused by infectious agents. More importantly though, your premise is fundamentally flawed: again, as you show yourself, cancer itself is an infectious agent (ever heard of metastases?). So why, then, is it usually not transmissible between individuals? Your answer doesn’t explain that at all.

@KonradRudolph I agree with you in that the original answer sounds misleading. Isn't it a moot point though? Fundamentally the transmissible agents that cause cancer (oncoviruses) are not themselves cancer. Metastatic cancers are not transmissible cancers either...

@GoodGravy No, it’s not a moot point at all, because it doesn’t explain why cancers generally aren’t transmissible, and that was the whole question. (I also disagree with your edit, since it changed the answer substantially, and such edits are frowned upon on Stack Exchange – you should have written your own answer instead.)

@KonradRudolph I see your point. Re: edit - The fundamental answer wasn't changed too much I don't think; I removed an erroneous statement and added in the missing information in a clause along with an order reshuffle. The answer was confusing and contradictory, now its not. If this was several separate edits would it have been okay? Remi.b can roll back if they want to.

The sentence "Some cancers are caused by infectious agents" come from an edit from GoodGravy, not from me. Note, also that the edit came after the downvotes. I re-edited the answer. Please let me know if there is still something going wrong. Thanks Konrad for your feedback.

There is a very obvious answer that is missing. Cancer is a disease of the cells of multicellular organisms, and the cells of multicellular organisms evolved away from the ability to live independently. With out the proper growth medium and in the case of mammalian cells, the permissive temperature, the cells of multicellular organisms survive for only short periods of time when outside of the body. Unlike bacteria, fungi, and unicellular protists, that are equipped to survive in an external environment, the cells of multicellular organisms need the multicellular organism's systems to survive.

@AMR I couldn’t find times of survival of individual (cancer) cells outside of medium. But plenty of bacteria and viruses die almost immediately outside of their host, and are still communicable by touch (prominent example: ebolavirus). I believe bacteria are generally more resilient but many are also quite particular about their growth medium and will just up and die when left alone. In other words: I think you vastly overstate the difference in survival between cancer cells and viral and bacterial pathogens. I don’t think this specifically is what distinguishes them: Immune response is.

@KonradRudolph You cannot make an immune response argument as the reason why cancers are not communicable when in 99.9999% of every cancer in human history and all but two species of highly inbred mammals are non-transmissible. You are not going to develop cancer because you prepared the body of a family member for burial who has died of cancer; You almost certainly will develop ebola. You can have sex with someone with prostate cancer and you will not get cancer. You might get HPV which could lead to cancer, but you will not develop cancer from the cancer itself.

@AMR Immune response is the reason why they’re not communicable. That’s my point. All of the cases you’ve just listed actually contradict your survivability point, since they all rely on transmission in which cancer cells wouldn’t need to stay alive outside the body. Incidentally, I hereby acknowledge that there may be other reasons besides immune response. But I don’t know of them, and they certainly haven’t been mentioned yet here.

@KonradRudolph No. Cancer is not communicable because it has no ability to act as an infectious agent. Period.

@AMR You are still begging the question. You are saying, in essence, “cancer is not an infectious agent because it is not an infectious agent” — Not quite, but it’s simply not an answer. The question is why. You are systematically evading this.

Naïvely, there’s no reason why cancers wouldn’t be communicable. Tumours consist of abnormally multiplying cells which have switched off their response to repressive stimuli from other cells, which would otherwise cause them to stop growing (plus a few other properties which have first been collectively described in the seminal paper The hallmarks of cancer).
And tumour cells can absolutely split off and start growing elsewhere, thus effectively spreading the cancer. This happens in metastases, and it happens in the few types of communicable cancer that are known.
So why does this normally not happen between individuals?
The reason is our immune system. Our bodies are normally incredibly good at recognising and eliminating foreign bodies – so-called antigens. The problem with cancers is that they are not foreign bodies: they are our own cells, only mutated. This makes it hard for our own immune system to recognise them as foreign. (It’s worth noting that at some point tumour cells have accumulated enough mutations to be recognised as foreign, but by this point the tumour is already mounting an effective resistance to the immune system.)
It’s for this reason that most cancers are not transmissible: invading cancer cells are immediately recognised as foreign bodies, and are efficiently eliminated by the immune system before they can multiply into a tumour. Unlike other antigens they have not evolved effective ways of evading the host’s immune system.
— Let’s take a detour here and talk about organ transplantation: When a donor organ is transplanted into a new host, the host recognises this organ as foreign, and initiates an immune reaction against it (or vice versa). This transplant rejection is a huge problem, and needs to be addressed by finding a closely related donor, and administering immunosuppressant drugs.
Which brings us back to transmissible cancers: all known types of transmissible cancer occur in species which have gone through a recent population bottleneck. All now-living individuals are very closely related. As a consequence, their immune systems don’t necessarily recognise another individual’s cells as foreign, or at least produces a reduced immune response.

I'd find it useful to add that in experiments where we're xenografting cancers for experimentation, in mice for example, we're often using something immunosuppressed like  RAG−/−γc−/− so the cancerous cells aren't destroyed by the immune system.

@Kendall I have to admit that I don’t know anything about that, but please feel free to add your own answer and/or edit mine. Also, thanks for this interesting piece information, I didn’t know that.

Comparing metastatic cancer to a communicable disease is a spurious line of reasoning. I would argue that you cannot even make the case for transplant related transmission, as part of the treatment protocol is the suppression of the recipients immune system, allowing affected donor tissue to spread. Most cancer cells are not like protists or bacteria which can survive outside the body for extended periods of time without growth medium.

@AMR Please explain why you find the comparison spurious — I don't understand that at all. It's also patently contradicted by the existence of communicable cancers. And the lack of survival outside the host is in no way relevant for the comparison I'm making. At any rate, many pathogens (both bacterial and viral) have the same problem.

You have three examples in all non-human mammals and all of the human examples are iatrogenic and you want to classify cancer, a disease that affects millions of humans and countless other organisms annually with no evidence of interorganism transfer, as a communicable disease simply because it evolves genetic expression patterns that give it gain of function mutations to move to other location within the same organism, then that is a spurious argument. An infection that spreads to a different area of the body is not a communicable disease either, it is a complication of the disease process.

@AMR No, I do not “want to classify cancer as a communicable disease”. I’m explaining why it isn’t communicable by considering what distinguishes it from other diseases (which are communicable). Explaining differences this way is a common teaching technique which apparently backfired here. But I’m not really sure how to improve that—maybe put the third paragraph in bold? Incidentally, the misunderstanding seems to be related to your use of the word “compare” as if it meant “claim that they are equivalent” when, in reality, “compare” just as well may mean “contrast”. That’s what I’m doing

@AMR Put differently, since there are tumours that are communicable (no matter how few), we must ask ourselves: “what makes cancer non-communicable in general?” The other reply, which just says that “cancer is not a pathogen” isn’t answering the question, it’s begging the question. By contrast, my answer actually explores the specific difference between pathogens and tumours. This is fundamentally different from claiming that they are the same.

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


text:
How do butterflies defend themselves from other creatures when they don't have the ability to sting or some other offensive/defensive mechanism?
How do butterflies defend themselves from other creatures when they don't have the ability to sting or some other offensive/defensive mechanism?

Butterflies are part of the class of Insects in the order Lepidoptera. Adult butterflies have large, often brightly coloured wings, and conspicuous, fluttering flight.

Hi there, I downvoted your question because its important to include an attempt at an answer in your question. Hopefully @fileunderwater gave you the answer you were looking for :)

It might come across harsh @ShyamRadhakrishnan especially as a new user, but you'll get used to it and eventually understand why!

Butterflies have a number of defence mechanisms, even if they don't have the ability to sting (as adults - see spines in larvae below). Here is a non-comprehensive list of some defensive mechanisms:

Toxins or repellents, which can be present in both adults and larvae.
Aposematism (warning coloration)
Mimicry, both in the form of resembling other poisonous species and using features such as eyespots.
Spines, bristles or long hairs, often in larvae (see google images), to make ingestion highly unpleasent or dangerous. See the Pine processionary moth (Thaumetopoea pityocampa) for an nice example of defensive larval hairs.
Camouflage/hiding
Sound clicks used to startle or disorient predators. This is most often known from moths to prevent bat attacks (see e.g. Cycnia tenera and Fullard et al, 1994).
Conspicuous features at the edge of wings to make them targets of attack, e.g. eyespots or appendages, which are used to lure predators to attack non-essential body parts (see Olofsson et al, 2013 for an example).

Nice answer! I removed my comment from the question as this says it all. +1


text:
Hot water bath and Infertility
From here:

Effect of temperature. Sperm cells will not mature at core body temperature in most mammals (spermatogenic DNA polymerase b and recombinase activities exhibit unique temperature optima); to adapt, the testes assume an external position. Testicular descent from the abdomen normally transpires during fetal or neonatal life.
If the testes fail to descend into the scrotum, a condition called cryptorchidism, the male will be sterile; gone uncorrected (by surgery or androgen treatment) spermatogonia will eventually degenerate.

How many minutes of exposure to hot water is tolerable?
Can regularly bathing in hot water lead to infertility?
Up to what temperature (of bath water - assuming the maximum tolerable temperature would not hurt skin) is tolerable?


text:
Is it a medical condition to not able to recall the word in a language while having a conversation
While having a conversation it happens to some peopl that clearly they know there exists a perfect word to be used but can not recall it during the conversation in real time and hence forced to use some other word which may not be so perfect.
But after the conversation is done they will be able to recall it. This happens very frequently to some people. Is this some kind of medical condition. If yes what is the name of this condition called as. ?

Welcome to Bio.SE! Thanks for your question. Self-help questions are strongly discouraged, so as to stimulate folks to seek professional help where necessary. Please remove any self-reference, otherwise the question may be closed. Secondly, it may be wise to post this question on Cognitive Sciences.SE as it may attract more attention there.

@ChrisStronks Thanks. Removed the self references

Have you read anything about any kinds of memory loss? Most accurately: maybe it is an illness, maybe it isn't.

@anongoodnurse Or may be it is a resultant of cannabis :P

The phenomenon you describe is known as tip-of-the-tongue phenomenon, where you know there is a word, and you feel it's "right on the tip of the tongue, but doesn't come out".
The phenomenon is normal and tends to worsen with age. Only in case it becomes so strong that it seriously interferes with daily life, it can be considered a medical condition (anomic aphasia) that may be indicative of damage to the brain, such as stroke, head trauma, dementia, or tumor.


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How can I reduce the background gradient in phase contrast microscopy?
I'm looking for ways to set up a phase contrast microscope to reduce the brightness gradient that appears across the background of my images.
I use phase contrast to find the outlines of cells in my images. My problem is that the automated processing algorithms I use get confused by strong brightness gradients in some images. Post-processing of the images disrupts the continuous nature of the histogram, again throwing off the algorithms.
Does anyone know why these gradients appear and how to reduce their formation?
Thanks,
Oliver
Edited the question to clarify that I am interested in microscope usage, rather than image manipulation
Sample image:

The image background is darker at the left of the image than at the right

Are you using the images to count cells or to determine shape, volume etc? Also, the question is borderline off-topic since it is mostly about image manipulation, so it would probably be good if you added some more info on the biological background/problem you are studying.

@fileunderwater I use the phase image to create ROIs for collecting data from epifluorescent images. How I use the images is not particularly important with respect to the question, though. I'm just interested to know if there are ways to configure my microscope such that the brightness gradient across the field is less pronounced.

Add this information directly to the question by editing. For the record, I think the question is fine since its an important lab techique (but I cannot answer it), but it might attract close-votes for being "only" about microscopy and not biology.

I hope not - there isn't a microscopy stack exchange I can post in instead! The biology exchange does contain many other questions purely related to microscopy, though... Furthermore, I expect biologists to comprise the largest demographic of microscope users, so I'm more likely to find an answer here than anywhere else. Thanks for your comments, I've edited the question accordingly.

Is it possible to provide an image of the problem?

I've edited the question to include a link to an image.

What's the microscope your using? Have you tried adjusting the condenser??? Also check your apertures.

It can be because of a silly error of a partially closed lens (the knob that lets you switch from camera to binoculars). That happened to me once.

Have you tried imaging an emptry slide and use it as background? (i.e. subtracting it from your image)

That's a good idea, @nico - I'll try it next time.

@WYSIWYG (and rhill), I have a similar problem sometimes where the condenser on our leica scopes can slide and doesn't always fully engage, but that's not so subtle (it completely disrupts the phase contrast effect). If anyone reading this is having trouble getting phase to work, the phase condenser is a fairly common cause.

If you're not already doing so, make sure you set up Kohler illumination every time you use the microscope -- see this tutorial by Steven Ruzin.
The lamp or the phase ring may be misaligned. There are usually small hexagonal set screws on the lamp housing and the condenser, respectively, to adjust these.
Imaging near the edge of a dish or well can lead to uneven illumination as the light is bent by the walls of the culture vessel. If this might be the cause, try re-doing the Kohler illumination before you take each image.
If you can't find the cause of the problem, there are several ways to correct for uneven background described here. Maybe one of them will work with your analysis.

Excellent first post! Welcome to Biology S.E.! If you need any assistance, please visit The Help Center.


text:
How to study the number of herbivores per type of tree and time of day?
Suppose I want to find out the number of herbivores in different kinds of trees, and also compare the numbers between day and night. How would this kind of study be run in practice? It easy to think of several possible confounding factors, such as the health of the trees, weather, etc.
If the trees are big, it is also difficult to find every living thing from that. One could of course then count the number of herbivores per defined area but again, picking the area should be carefully controlled.
From a statistical perspective, I can just make an estimate of expected effect size, and calculate the sample size that is about enough for detecting possible differences in the above mentioned conditions. However, I find these other aspects very difficult to do... All help would be appreciated :)

I think there are a lot more factors you need to provide before someone will give you a helpful answer. What trees are these, what herbivores are you studying for example?


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How to preserve leaves between sampling (collection) and analysis?
Suppose I spend a day in a forest, collecting different kinds of leaves, which I would like to analyze under a compound microscope. Now, obviously, measures should be taken to preserve the leaves some how. What would be the appropriate procedure? It seems (based on browsing the web..) that refrigeration could be one option. Is it scientific (used in published papers)?

What is the aim of the analysis and what type of traits/features do you want to study?

You may want to see:
Mark W. Chase, Harold H. Hills; Taxon, Vol. 40, No. 2,  1991, pp. 215-220: 'Silica Gel: An Ideal Material for Field Preservation of Leaf Samples for DNA Studies'
Summarized, the process would be the following:

Place the leaves inside ziplock plastic bags;
Add ten times (minium) the weight of the leaves in silica gel;
After 12 hours (after which the degradation of the biological material is more likely), check the leaves by bending them: if they break cleanly, the leaf is dry;
Store in the ziplock bag, inside a box with an hermetic lid;
Refrigerate (if possible).

Note: Freezing by submersion in liquid nitrogen is also a viable approach, yet might be less practical

I was thinking about the same thing with regard to DNA (have used it myself previously), but it sounds like the poster wants to analyse morphology.

This method (although I haven't ever used it, or seen it in use) seems to preserve the shape and physical features of the leaf, essentially "freezing" the leaf. In fact, a quick search for images will show that the biological material is kept more or less intact.

Placing the leaves in wax paper and under the pressure of several books would be beneficial (in terms of a short term preservation).
This method may not be suitable for field preservation, due to the bulky nature of books and other weights, although it might be suitable if using an alternate method of pressure.


text:
Name (and meaning of the absence) of the white semicircle at the base of the fingernail?
At the base of fingernail, there is a white semicircle (see on the first picture). But sometimes there isn't one.

My questions are: what is this white semicircle on the fingernail, and what causes it? What is the explanation when there it isn't on all of the fingernails (see on the second picture)?

The lighter crescent-shaped part at the base of the nail is called the lunula. It is a normal part of the nail matrix, and indicates nail growth. The faster your fingernails grow, the more obvious the lunula.

Absence of the lunula without any other abnormalities of the nail is not uncommon, and while it can indicate anemia or malnutrition, it is often found normally, and with aging. In this case, careful inspection of all the nails will usually reveal a lunula on the thumbs and the fingers closest to the thumb, but a very small or absent lunula on the other fingers.
In your picture, there is clearly a lunula on the middle finger, and, I suspect, a larger one on the index finger, and a relatively normal one on the thumb. This is not a finding of great concern in the absence of other pathology.

The lunula: The small, whitish, half-moon shape that you sometime see at the bottom of your nails is called the lunula(pronounced loon-yoo-la). It's actually part of the matrix. You might be able to see it only on your thumbs, or maybe not at all. Don't worry if you can't see a lunula on any of your fingers. It's no big deal. It's there, just under your skin.

Examining the Fingernails When Evaluating Presenting Symptoms in Elderly Patients
Examining the Fingernails
Nails


text:
Is there a biological environment that we can we assume glutamate exists as glutamic acid?
In the body we almost always assume that glutamate exists as glutamate rather than glutamic acid. It is so commonly glutamate yet glutamic acid and glutamate share the abbreviations of Glu and E. From the wikipedia page:

The side chain carboxylic acid functional group has a pKa of 4.1 and therefore exists almost entirely in its negatively charged deprotonated carboxylate form at pH values greater than 4.1; therefore, it is negatively charged at physiological pH ranging from 7.35 to 7.45.

Glutamic acid:

Glutamate:

Given that the pKa of glutamate is 4.1, is their any biological situation (a cell type, organel etc.) that glutamic acid is preferred?
Additionally, does this have any large biochemical implications, or is that outweighed by the (relatively speaking) "extreme" acidic environment?

I'm confused by your question. Glutamate predominates at physiological pH.

Completely got them mixed up as I was writing, whoops! The underlying point is "where does the protonated form occur biologically, and does it matter?"

I figured as much. I might search for some examples later, but here's some speculation on where you might find it: proteins naturally found in the digestive track, acidophiles, active sites during catalysis. 4.1 is the pKa of glutamate free in solution. In a protein, this can change depending on interactions with other residues.

http://onlinelibrary.wiley.com/store/10.1111/j.1432-1033.1995.0839a.x/asset/j.1432-1033.1995.0839a.x.pdf;jsessionid=13F89FDABD001B72EC378584D072499C.f01t02?v=1&t=i5tvptqb&s=4913cff97a3d52693972c1e0917f3222bd9c67f4

lysosomes, stomach acid.

At typical physiological pHs glutamate does exist as glutamate.
Broadly the acidity in the digestive track is enough to reduce glutamate to glutamic acid. The stomach for example has a healthy pH of between 1.5 to 3.5.
Canadianer points out in the comments that the active site during catalysis are protonated. There are obviously a lot of examples of this and sensitive evaluation by looking at the isocontours and surface potential of the protein structure are needed to draw conclusions if this might be important.


text:
Does long term use of antibiotics in humans actually lead to a greater risk of infection?
I've read about the overuse of antibiotics leading to antibiotic resistant strains of bacteria, so generally does long term use of antibiotics breed these strains in the bodies of antibiotic users and increase the risk of various bodily infections?

Not usually in the individual, but in a population, improper antibiotic use can lead to resistant strains and more infections. Improper use usually means stopping therapy short and not using all the pills, using antibiotics for diseases they cannot help with, or very-long-term use in a healthy individual. Antibiotic resistance is basic a probability function, with the increase exposure to the antibiotics increasing the probability resistance will develop. Regimes are designed so that bacterial populations stay isolated/small and the chance for resistance remains small.

Not really your question but another problem of an overuse of antibiotics, is that there are many bacteria in your body especially in your digestive system which are important to stay healthy but are also killed by antibiotics. To get these bacteria back into your body there is a discussion about "poo pills"

does long term use of antibiotics breed these strains in the bodies of antibiotic users[,] and increase the risk of various bodily infections?

Yes to the first question (although I would use the words select for). No, not usually for the second question in the individual(*), yes in the population.
This should be looked at as a problem in populations of both people/animals and bacterial populations in general. Given time, any living organism will be favored if a mutation involving a selective pressure (like an antibiotic) is introduced, not only in those towards which the antibiotic is directed but also among the normal microbiota. The longer the selective pressure (antibiotic treatment), the greater the probability that a resistant strain of one bacteria or another will develop.
That's why there's a push (in studies) to limit the number of days of antibiotic use necessary to the least number needed which still proves efficient in eradicating an infection. (The trend is towards kill 'em quick and kill 'em all - higher doses for shorter periods, or make it strong and only long enough to cause the extinction of the illness-causing bacteria and not long enough for selection of resistance mutations.)
It is quite normal to have potentially pathogenic bacteria as part of one's microbiome. Usually other beneficial bacteria and conditions keep these in check. But antibiotic resistance, once selected for, can persist for longer periods of time than previously recognized (up to four years in one study). This gives even a small population of resistant bacteria to genetically transfer resistance to others.
Short-term use is less likely to select for resistance in one individual, but, in terms of populations of people, antibiotics are used so ubiquitously that resistant strains will be selected for in shorter treatment intervals by sheer numbers of people being treated.

When resistant and susceptible organisms compete to colonize or infect hosts, and use of an antibiotic has a greater impact on the transmission of susceptible bacteria than resistant ones, then increasing use of the antibiotic will result in an increase in frequency of organisms resistant to that drug in the population, even if the risk for treated patients is modest. Antimicrobial use and patient-to-patient transmission are not independent pathways for promoting of antimicrobial resistance, rather they are inextricably linked.

"Long term use" in one individual is relatively uncommon and unnecessary, but if necessary, usually does more good than harm to that individual. Almost all (if not all) of the population of the bacteria you're trying to eliminate from one site will be susceptible to the antibiotic and will die, leaving, in a few cases, a few resistant ones that your body can handle naturally, or that can repopulate to "normal" levels without causing illness. But they are then there, the resistant ones, to spread within a population of the individual's microbiome, and the population of people. The next person with a problem, who might have picked up that resistant strain, will not respond well to the same antibiotic. Nor will the patient who was initially treated, if the problem recurs with an antibiotic resistant strain. So, as I said, yes and no.
That's why people (doctors, vets, and - with help - patients) should consider a risk-to-benefit-ratio whenever using an antibiotic. From that standpoint, it is always unethical to use an antibiotic for what is probably a virus, because the benefit to a patient is very small, but the risk - to that patient, who might suffer complications from its use, and to the population if a resistant strain is selected for - is relatively high. Better to wait it out to see if it is bacterial (if one can't test for it directly), and treat it if it does turn out to be. Of course, the risk of not treating in certain populations must also be considered: the elderly, the immunosuppressed, infants, and people with other illnesses or predispositions to infection.
It's not just use of antibiotics in patients/humans that causes problems; its use in any situation can lead to selection for resistance. This is well documented to occur in the meat industry, where a grower often tries to minimize the effect of cost-efficient but insalubrious growing conditions by giving antibiotics to the entire population of meat-animals (beef or poultry) to cut the monetary losses associated with potential illnesses.
It's a multifactorial, and often monetarily driven, problem. Doctors share the blame, but so do patients who demand antibiotics thinking they know better than the doctor, and who will doctor-shop until they find one who will do their bidding, or make a stink for the doctor who refuses. Some doctors still refuse, but they pay a heavy (non-monetary and sometimes monetary) price for doing so.
In the meat industry, it's always a monetarily driven process.

This review focuses on agricultural antimicrobial drug use as a major driver of antimicrobial resistance worldwide for four reasons: It is the largest use of antimicrobials worldwide; much of the use of antimicrobials in agriculture results in subtherapeutic exposures of bacteria; drugs of every important clinical class are utilized in agriculture; and human populations are exposed to antimicrobial-resistant pathogens via consumption of animal products as well as through widespread release into the environment.

What YOU can do:
Do not take an antibiotic for a viral infection like a cold or the flu.
Do not save some of your antibiotic for the next time you get sick.
Take an antibiotic exactly as the healthcare provider tells you. Complete the prescribed course of treatment even if you are feeling better. If treatment stops too soon, some bacteria may survive and re-infect.
Do not take antibiotics prescribed for someone else.
If your healthcare provider determines that you do not have a bacterial infection, ask about ways to help relieve your symptoms. Do not pressure your provider to prescribe an antibiotic.
Antibiotic resistance: delaying the inevitable
Get Smart: Know When Antibiotics Work
Short-Term Antibiotic Treatment Has Differing Long-Term Impacts on the Human Throat and Gut Microbiome
Antimicrobial Use and Antimicrobial Resistance: A Population Perspective
Comparison of 8 vs 15 Days of Antibiotic Therapy for Ventilator-Associated Pneumonia in AdultsA Randomized Trial
Plasmid encoded antibiotic resistance: acquisition and transfer of antibiotic resistance genes in bacteria
Industrial Food Animal Production, Antimicrobial Resistance, and Human Health


text:
How do I find a protein from this DNA sequence?
I have a DNA sequence from a sequencer. How can I determine what protein is it? I tried some translator but it didn't help. What protein is this and how can I determine it?
The sequence: CGTTCTATAGATACGCGATGACGGTATACCATCCGCAAAGT
Thank you very much!

Have you tried to blast the sequence?

Translation would fail on this sequence since it’s not a complete open reading frame (doesn’t start with a start codon, doesn’t stop with a stop codon, and length not divisible by three). As such, we don’t even know whether it’s in frame, or maybe shifted by a nucleotide.

Entering fragment in BLASTX helped

Enter it in BLASTX. This will give you any protein sequence matches as well as likely homologues given a nucleotide sequence.

Great, I hope that was good news for you!

You might want to try searching against NR/NT database using BLAST. This way you will get to know what this sequence might be similar too. The length of the sequence is too short to code for any meaningful protein.


text:
What is some computer science technology that can help the development of biology?
What is some computer science technology that can help the development of biology(eg. artificial intelligence, resolution technology) and  briefly talks about their potentials?

This is an incredibly broad question. Computers are used for all sorts of things in modern biology that don't have anything to do with genetic engineering.

The question is very broad and it is impossible to correctly answer to it. I think you may not realize how much computation is everywhere.
Here is a bunch of things for which I personally use modern computation power

Population genetics simulations
Simulations of developments (Gillespie algorithm and variants)
Statistical analyses, incl. some analyses that are a bit demanding such as permutations test, bootstrap or maximum likelihood
Numerical approximations to mathematical equations that can't be solved analytically.

Many people make good use of computation in biology for treating DNA sequence data (annotating sequences, aligning sequences, comparing sequences, building phylogenetic trees). Typically this kind of task can be extremely demanding. I know a lab who uses Blue Gene in order to perform statistical analysis on sequence data. Some people simulate brain activities. Some people simulate the physics of molecules, some people simulate blood flow through the body while others simulate how a new substance injected in the body spread. and it goes on and on... This list is probably biased toward my field of expertise.


text:
What is the meaning of dots and dashes in clustalw?
I am converting outputs in stockholm format to clustalw using
Bio::AlignIO->new(-file => "$ARGV[0]", -format => "stockholm"); and

Bio::AlignIO ->new (-format =>'clustalw');

I am also using
my $new=$aln->remove_columns(['all_gaps_columns'],'.');

and got an output like
head1  ----------------.GG-.-gggaguggugugguuacgaaugUGGCCUCUGC-----A

head2  GGGGGUGUAGCUCAGU.GGU.A......................GAGCGGAUGCUUUGCA

What is the meaning of dots and dashes? Is this natural in a clustalw output? Am I getting a bug?
I was unable to find the sequences I used in the original message but these two pose a similar pattern. These are RNA sequences, including pseudogenes, so there are lots of palindromic sequences.
# STOCKHOLM 1.0
#=GF AU Infernal 1.1.1

head1          --------UGGAGAAU.G--.-ugggcguc.gaucccacUUCCUCUCGCAUGCUAA..............................................................GCGAGC-gcucuaccacuugagcuaauucccc-..-------------..................................
 #=GR head1 PP ........89999988.4....6789****.********999**************..............................................................******.7999999866665555555554444..................................................

 head2         --------UGGAGAAU.---.-gcgggcaucgaucccgcUUCCUCUCGCAUGCUAA..............................................................GCGAGCG.........................-..-------------cucuaccauu........................
 #=GR head2  PP ........89999887......46789************9999*************..............................................................*****86.........................................4555666666........................

 CLUSTAL W (1.81) multiple sequence alignment

 head1  --------UGGAGAAU.G--.-ugggcguc.gaucccacUUCCUCUCGCAUGCUAA....
 head2  --------UGGAGAAU.---.-gcgggcaucgaucccgcUUCCUCUCGCAUGCUAA....

Dash is used for gaps and dots are used for semi-conserved substitutions (similar residues). But this looks weird. Are you sure this is how you got the output because the dots are present below the alignment (next line)?

Sorry for putting this in the Answer box, but I don't have enough rep to comment yet... Can you please post the contents of your stockholm file as well? Also, just to be 100% clear, you are using BioPerl for your conversion, yes?

This looks like you are running clustalw with bioperl. I have answered assuming the original alignment is wrong. Could you post your original alignment, and what versions of these are you using?

Please show us the sequences you are attempting to align. They look like low complexity regions which are very hard to align but we can't judge without seeing the originals.

Yes, I am using Bioperl. I uploaded a sample of the original.

As WYSIWYG touches on in the comments, usually dashes mean that there are gaps in the alignment as the result of an indel event. Dots are used to show specifically point mutations where the biochemical properties are mostly conserved, but the residue has changed.

From original question, not relevant to question as it stands.
You are right in that this isn't a proper alignment, however I'm not sure it is a bug. What you have appears to be the alignment of a nucleotide sequence that has gone horribly, horribly wrong.
As a first guess without any more details I would say it doesn't look like you have installed clustalw correctly or pointed your bioperl to it. From the documentation here are common problems:

Make sure the clustalw executable is in your path so that
  which clustalw
  returns a clustalw executable on your system.
Define an environmental variable CLUSTALDIR which is a
  directory which contains the 'clustalw' application:
  In bash:
export CLUSTALDIR=/home/username/clustalw1.8
In csh/tcsh:
setenv CLUSTALDIR /home/username/clustalw1.8
Include a definition of an environmental variable CLUSTALDIR in
  every script that will use this Clustalw wrapper module, e.g.:
BEGIN { $ENV{CLUSTALDIR} = '/home/username/clustalw1.8/' }
  use Bio::Tools::Run::Alignment::Clustalw;

Unless you are doing massive amounts of sequence alignment, the clustalW2 webserver is quicker, more sensitive and way easier to use.

Based on the edit you made to your op, the dots are present in your initial stockholm alignment, and are simply being copied into the new clustal output.
What is the source of your alignment to begin with? I'm assuming you're selecting individual rows from a larger alignment, given the odd distribution of gaps. This could give you a clue as to the actual significance of the dots (dashes are pretty much always gaps).
Also, just fyi, if you want a command line tool to do the conversion for you, I have a python3 module called SeqBuddy that will work just fine. You'll need BioPython as a dependency though.
$: python3 SeqBuddy.py input.stockholm -sf clustal > output.clustal


text:
By what method do ants dissect and hold soil
Not sure if this is the correct stackexchange site - please migrate/advise as you see fit.
I'm interested in the method by which ants "break off" a small amount of soil and then hold it in their jaws (?).
To clarify I know ants break off soil in small quantities, so that a single ant carries very little soil; I'm interested to understand what exactly how this happens. For example does the ant literally pick the soil directly, or does it brush it loose first etc. Further to this I'd like to know how the ant holds the soil. Is it akin to the soil being atop a palm, or more like being held between two hands?
Broader context: I'm looking into making a model of this type of soil movement and I wanted a more detailed understanding.

This is definitely on-topic here @FraserOfSmeg

Short answer
Ants use specialized facial structures called mandibles to cut, shape and carry soil and other matter.
Background
you say "I know ants break off soil in small quantities, so that a single ant carries very little soil...". On the contrary I would say - Ants can carry relatively a lot of soil, as they can lift up to about 100 times their own body weight. In absolute terms, however, the weight carried is about 500 mg (Spectrum).

Source: The World's Best Photos
The structure that ants use to break off and carry soil are their mandibles:

Source: Tree of Life Web Project
Mandibles are specialized bodily structures typical for insects, and I quote from the University of Sydney website:

The mandibles are the first pair of jaws in insects, moving laterally (i.e. from side to side) when in use. Mandible shape is strongly influenced by function and is therefore highly variable. For example a chewing insect will have strong tooth-shaped mandibles while in a sucking insect they will be thin and needle-shaped. Mandibles are used to cut, chew and tear food as well as to carry objects, fight and mould materials such as wax or soil.

thanks for the thorough answer. Could you help me understand how the ants don't squash (and then drop) or knock soil lose? In every video I've seen they seem to have almost unbelievable precision!


text:
Why does uterus have to be prepared every month for fertilization?
I'm just curious why it has to happen every month when the uterus could have been prepared from the beginning and kept that way throughout life or till a certain point. But why make and break it every month? (The breaking of this preparation is the cause of menstrual pain, which is what I'm worried about).

Welcome to Biology S.E.! If you have additional questions please visit The Help Center

You may be interested in estrus

A quick search through the Internet, as well as any textbook, will reveal that the lining of the uterus (endometrium) created thickened during every menstruation cycle is rich in nutrients, and requires a constant blood supply, in order to accommodate a fetus.
Therefore, maintaining the lining would be more costly to the body than rebuilding it every month; in fact, as part of the lining is reabsorbed, rather than destroyed and expelled, thus conserving energy and nutrients. The reason a part of the endometrium is not reabsorbed is its thickness, which prevents its total reabsorption.
Also, the menstrual pain is, in fact, caused by the breaking down of the endometrium, although not directly, but by muscular contractions (cramps) and the contraction of blood vessels, which happen to prevent blood loss and help with the expelling of the endometrium.


text:
Do these things contain amylase?
I have 10 samples of some food or other things and I need to know, if it contains amylase. I already ran an experiment with storch and iodine, but I have to make it right and my experiment must not be right.
List of samples:

Saliva (I know this one)
Banana peel (inner side)
Corn
Sponge biscuit
(http://www.kaloricketabulky.cz/fotografie-velka/f1136aba2e11082a/piskoty-detske-kulate.jpg)
Tomato
Banana (dried)
Bread
Potato peel
Ketchup
Milk

Thank you very much!

What was the problem with your experiments? You can't trust your results, why?

Because I dont know if I did it right. And for example potato peel colored something between iodine without starch and iodine with starch.

This sounds like a piece of homework. An important thing to learn in science is that you have to take the results for what they are - though the experiments should be arranged so that they could convince you i.e. repeating 3 times or something similar. Negative and positive controls are used to test whether you did it right. http://en.wikipedia.org/wiki/Scientific_control#Negative

you can also compare your results with that of your fellow students to improve reliablity and eliminate subjective bias

Amylase is an enzyme that breaks down starches to simpler sugars. Only living organisms can produce amylase. Animals produce only alpha-amylase. Plants, bacteria, and fungi produce both beta- and alpha- amylases. Like all proteins, the presence of amylase in food depends on if it is permanently denatured by high enough temperatures or extremes in pH. Interestingly, amylases can be classified into high/intermediate/low thermostability groups, depending on whether they become inactivated at a certain temperature. Taking this into consideration, saliva would definitely have alpha-amylase. Bread and biscuits may have alpha or beta amylase (depending on baking temperatures/pH, if amylase was added at all, and if it comes from a grain). Of the rest of your list, banana, corn, milk, and sweet potato would have amylase. Honey (not listed) would also have it. Tomato seems to amylase activity as well. For ketchup, it seems to be an added ingredient to speed processing.
Sources:

http://www.gmo-compass.org/eng/database/enzymes/80.amylase.html
http://www.lallemand.com/BakerYeastNA/eng/PDFs/LBU%20PDF%20FILES/2_7SOFT.PDF
http://www.ehow.com/info_12013063_plants-contain-amylase.html
http://www.ajofai.info/Abstract/Detection%20of%20amylase%20activity%20from%20vegetables%20and%20fruit%20in%20an%20undergraduate%20classroom.pdf

but yeast zymase is not amylase?

@CRags, yes you are right! yeast can make amylase too though, I believe, but zymase is the more active enzyme in yeast. bad example then on my part.

I didn't know yeast can make amylase. Thanks for the info. Thinking on banana, it makes sense if amylase is present in it (as it's sweet, it must have a lot of glucose).


text:
What flower is this blue flower?
What flower is this?  All help would be appreciated

Could you add further information as to e.g. where you found it?

Was it spray-painted blue? Do you have a picture of the whole plant? Thanks!

Do you have an image which shows the whole flower (ideally with some leafs)?

Species identification questions are on topic as long as sufficient details are provided. This question does not have enough details.

Without more detail about the whole plant (including leaves), where it came from, and about whether or not it was spray-painted, watered with dyed water, etc. it would be difficult to ID.
It seems to be in the Asteraceae family, and in the pompon class, as seen in these vender's pictures. (Disclosure: I have no affiliation with the company.)
http://www.fiftyflowers.com/product/Blue-Cushion-Bulk-Flower_10.htm
http://www.fiftyflowers.com/product/Blue-Cremon-Bulk-Flowers_24307.htm
http://www.fiftyflowers.com/product/Electric-Blue-Flowers_10.htm
It is most similar to a blue chrysanthemum.

http://john-hallett.co.uk/2013/04/04/blue-crysanthemum/

Sources:

as listed above for images
http://en.wikipedia.org/wiki/Chrysanthemum (pink image)
http://www.mums.org/chrysanthemum-classes/