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Mass spectrometry versus western blotting for validation
I have mass spectrometry data (LC-MS/MS) from rat cortices under either drug or control treatments. The results were performed in triplicate (three pairs of rats, drug or control per pair). In addition to some of the bioinformatics analysis I am doing, I will have to validate some of the fold-changes from the mass spectrometry by Western blot in order to have my results published.
Some of the proteins I have chosen to to validate work very nicely by Western blot which captures the same trend as the mass spectrometry. However, other proteins that I have attempted to validate go in the exact opposite direction.
My questions:

In general, how accurate is mass spectrometry compared to Western blotting?
Is it unusual to have a lot of variability between the results of the two methods? I am worried that I might have to try multiple proteins before I see the results replicated and this seems problematic to me. That leads me to the third question.
Which result should I trust?

Other information - Some of the proteins I have chosen for validation come from lower in the list where not as many peptide fragments were detected. In some cases, fragments were detected in only 2 of the 3 biological replicates. I did not chose to validate proteins where the 2 or 3 replicates varied widely in normalized spectral count values so I would expect these readings to be accurate. Additionally, the mass spectrometry part of the experiment was performed by a reputable lab that has filtered erroneous data using FDR cutoffs. There is a high correlation overall between all three replicates for a particular treatment and low standard error between samples across the population so, statistically, I trust the mass spec results.
If you need more information please ask - I don't know what exactly will be useful to answer my questions.
EDIT :
This article discusses the justification for using western blotting to validate mass spec results. It suggests using selected reaction monitoring assays as an alternative. Some of the points made by commenters in this thread are reiterated in this article.

Trying to answer any question other than "is this protein actually present in my sample" with a Western seems like a fool's errand. I think that it's completely reasonable to expect a large variability between your two methods.

@tel This is my thinking as well. However, the reviewers did not agree. In their comments they have asked us to follow up with biological validation, including Western blots that support the trends. I have looked at other mass spectrometry papers from this journal and they all follow their data up with Western blots that replicate the trend.

Ohhh, reviewers and their blots. I think that I have heard similar stories several dozen times now. Have you done replicates of the blots?

Yup, I've heard the same too. Each protein is 4 biological replicates (ie. from 4 homogenized rat brains) and each has 3 technical replicates. I'd like to do more but all these rats and antibodies are starting to add up...

My impression is that Western is the gold standard that MS is measured against, but not rightly so. As you have witnessed, it's perfectly possible for Western to fail because of eg. poor antibodies when MS will perform fine. It is not necessarily better than MS. Generally, if MS and Western disagree, I don't think you should really just trust one (whether you would get away with it is a different matter). Either one could be an artifacts. Without additional experiments, it's very hard to say.

Make sure you're running your Westerns with the exact same samples that you're using for mass spec. You mentioned in your question that the MS samples were cortices, but you're using homogenized (total?) brains for the Westerns - there definitely could be differences in protein expression and regulation, as you're essentially looking at two different samples.

@ MattDMo I was not clear in my comment. The fractions of brain homogenized are identical between the Western blotting and mass spec (I am comparing the post-synaptic density in the two methods, not the total lysates). I have been running the same rats for the Western blots but from the other hemisphere. Unfortunately, the entire sample had to be submitted for the mass spec so I don't think there would be a way to run the exact same samples, but at least it's from the same rat.

It is a common practice to prove a result using an orthogonal technique. Like RNAseq followed by qRT-PCR etc.
Western blotting is not a robust technique and cross comparisons are difficult because of difference in the avidities/affinities of different antibodies. So comparisons can be made only with one protein-control pair in different conditions.
LC-MS is more sensitive and less biased(IMO). So the general trick is- don't do westerns for all proteins just report the ones that behave well (say that you "chose" these because they are important). I know this is a wrong practice and I should not be advocating it. For your own scientific validation try it with another MS technique; if you used ESI-Quadrupole/ion-Trap etc then try with MALDI-TOF or iTRAQ. Some luddites will continue to cling to westerns.
I think it is better to not test the proteins that have low peptide counts. See what is known as MA plot. This is frequently used for microarrays. Here M denotes fold change and A denotes total expression in both samples. Don't pick proteins that are low in expression in both samples; they might not be meaningful. For example if you have 2 molecules of X and 100 molecules of Y in control condition and 5 molecules of X and 200 molecules of Y in test; then the fold change in X would seem important; however this change may not be relevant and can be a result of stochastic fluctuation/measurement error. If you have many samples you can see if something is stochastic or not but the limitation is the number of samples.
Note: I am not saying that 2→5 molecule increment should be meaningless. But to know if they have a meaning or not you would require more complex models; better avoid them at this moment.

I mentioned in my original post that we sent our samples to another lab for processing and mass spec. They returned "normalized spectral count" data back to us. From what I have been able to gather, the MA plot would be utilized in obtaining these normalized spectral counts (though I am not sure what method(s) they used for normalization). If I understand correctly, I would need the raw data - not the normalized data - in order to generate the MA plot, is this correct? Lastly, I have read about volcano plots; would it be more appropriate than an MA plot?

@syntonicC Perhaps you can ask them what normalization they have done. It is certainly possible that the overall expression was low in a certain sample and this can be normalized so that the two samples are comparable (as in quantile normalization). Even then the low expressing ones will remain so. And you can remove them. You don't actually need to plot. You can use a general low expression protein (from knowledge) for comparison. I hope you have the entire normalized data including the non-differentially expressed ones.

@ WYSIWYG I have emailed the lab for the information on the normalization method. And yes, I have the full data set. Thank you for your information on the comparison, this will be helpful for me moving forward. Additionally, I found an article discussing some of the things mentioned in this thread and I've added it to my original post.


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Choosing appropriate statistical test for ordinal data
Ordinal response variables show up often in biology, but I'm not sure how they are best analysed. Some examples are qualitative assessments (little, many, a lot) or risk assessments (low risk, medium risk, high risk).
My study is about correlation between pain and depression levels. We are measuring pain on an ordinal Likert scale. This is a number scale running from 10 (severe pain) to 0 (no pain).
We will also measure depression on a similar scale (scale: 4 - 0).
What statistical test should I use?

This is perhaps better suited to math SE.

@canadianer This isn't suited to Math.SE, but Cross Validated (http://stats.stackexchange.com/)

This is suited I think, as Likert scales are (ab)used often in biomedical research.

@ChrisStronks the question is not about biology but the application of a statistical method. Your answer is excellent and would make a great addition to Cross Validated but I believe it is off-topic here.

@Luigi No wonder I couldn't find a statistics SE…

Mann-Whitney U test. (?)

I think this question could be useful to have on the site, since this issue can come up in many biological fields. It is clearly on-topic at stats.stackexchange.com as well, but this does not necessarily mean that it's off-topic here. The choice of methods/assumptions can also interact with the biological process you are trying to model, which is why I think it's on-topic here as well. If questions such as this one is closed, I think we need to close many of the other questions using the statistics tag for fairness.

Could do with information about the experimental design, whether it is a balanced design, sample sizes, and normality of the distributions, and hypotheses.

You can use ordinal multinomial regression (also known as ordered logit) if the response is ordered. These methods are basically extensions of logistic regressions, but using e.g. a cumulative logit instead of the logit. However, there are a number of different assumptions you need to consider. For instance, are you going to use a proportional-odds assumption (which is commonly used), which means that there is an equal probability of going from e.g. class 1 -> 2 and class 5 -> 6? You can also evaluate the proportional odds assumption using plots or a score test. If the response cannot be ordered, there are multinomial nominal methods that you can use, and you can also evaluate the results from an ordered analysis by comparing the predictions with ones from a multinomial nominal analysis. I have used these kinds of methods for the analysis is Red list classifications, which are clearly ordered but cannot simply be transformed into a numerical response (similar to your situation).
The book Analysis of Ordinal Categorical Data (Agresti. 2010) is a really good starting point.
In R you can look at the packages polr and vgam for ways to perform different types of analyses on ordinal data. The author of the book above has also published some examples for categorical data analysis in R, using the packages I mentioned: Examples of Using R for Modeling Ordinal Data. In SAS similar analyses can be done using Proc Genmod and Proc Logistic.

The testing of an ordinal scale requires non-parametric statistical tests. Mean and standard deviation are invalid parameters for descriptive statistics whenever data are on ordinal scales, as are any parametric analyses based on the normal distribution.
The report of Allen & Seaman, 2007 describes a number of possible tests:
Nonparametric procedures—based on the rank, median or range—are appropriate for analyzing these data, as are chi-squared statistics.
Notably, Kruskall-Wallis models can be used to replace a standard parametric analysis of variance, as it is based on the ranks and not the means of the responses. Given these scales are representative of an underlying continuous measure, one recommendation is to analyze them as interval data as a pilot prior to gathering the continuous measure.
However, non-parametric tests are notoriously low in statistical power. There is a way of making an ordinal Likert scale like the ones you use continuous by using a ruler or slider, see the following figure (taken from Allen & Seaman, 2007):

This trick makes it continuous and normal parametric tests can be used, ramping up statistical power substantially. It is a lot more work though to analyze the data. Especially when the subjects indicate their perceived pain/depression by physically putting a mark on a paper ruler, as you have to manually measure the responses. A digital slider can make your life easier. If you are planning to do hundreds of subjects you should carefully think about the possible options.
Good luck!

There are parametric tests for ordinal response variables, which are basically extentions of logistic regressions.

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Deciduous trees in tropical rainforest
Some books says the dominant plant form in tropical rainforest biome is broad leaved evergreen trees. Other books say it is broad leaved evergreen trees and deciduous trees. What is the most accepted way (or the truth)? Also how do you explain the deciduousness adaptation in tropical rainforest (e.g., when do they shed leaves)?

Please could you provide sources?

For example, Cain, Bowman, Hacker's ecology textbook [2nd edition] (ISBN 978-0-87893-083-8) says the latter (i.e., evergreen and deciduous trees).

Are you sure that both talk specifically about tropical rainforests? There is also temperate rainforest, where deciduous trees are common. However, there is also seasonal (eg monsoon) tropical rainforest, which have many/mostly decidious trees. I cannot say which types are most common overall though (as in area).

Deciduous trees are those which shed their leaves once a year at the time of winter season and later grow new leaves, plants those keep their foliage throughout the year are called evergreens. Deciduous trees usually have broad leaves e.g., ash, beech, birch, maple and oak. There is a confusion exists over the dominance of trees in rain forest, but most of the resources suggests broad leaf evergreen trees as the most dominant. But deciduous trees are equally important because the difference may be negligible.

Deciduous trees shed their leaves usually as an adaptation to a cold or dry season. Evergreen trees do lose leaves, but each tree loses its leaves gradually and not all at once. Most tropical rainforest plants are considered to be evergreens, replacing their leaves gradually throughout the year as the leaves age and fall, whereas species growing in seasonally arid climates may be either evergreen or deciduous.Reference

The dominant plants in the tropical rain forest are broadleaf evergreen trees. Unlike evergreens that grow in colder parts of the United States, those of the tropical rain forest have no protection against cold weather or droughts.Reference

Adaptations of Deciduous trees

Broad green leaves capture sunlight needed to make food through photosynthesis.
They cuts off the supply of water to the leaves and seals off the area between the leaf stem and the tree trunk, as sunlight and water become scarce, the leaves are unable to continue producing chlorophyll and this produce vibrant colors in the leaves.
In winter, they simply loose their leaves and seal up the places where the leaves attach to the branch. Losing their leaves helps trees to conserve water loss through transpiration.
In spring the trees grows back their leaves and start the cycle once more.

In the spring, deciduous trees begin producing thin, broad, light-weight leaves. This type of leaf structure easily captures the sunlight needed for food production (photosynthesis). The broad leaves are great when temperatures are warm and there is plenty of sunlight. However, when temperatures are cold, the broad leaves expose too much surface area to water loss and tissue damage. To help prevent this damage from occurring, deciduous trees make internal and physical adaptations that are triggered by changes in the climate.
Cooler temperatures and limited sunlight are two climatic conditions that tell the tree to begin adapting. In the Fall, when these conditions occur, the tree cuts off the supply of water to the leaves and seals off the area between the leaf stem and the tree trunk. With limited sunlight and water, the leaf is unable to continue producing chlorophyll, the "green" stuff in the leaves, and as the chlorophyll decreases the leaves change color. The beautiful display of brilliant red, yellow, and gold leaves, associated with deciduous forests in the fall, is a result of this process. Most deciduous trees shed their leaves, once the leaves are brown and dry.
Reference

authors: Анастасия Долинская

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Action potential changes in low sodium concentrations but constant osmotic pressure

If I bathe a squid axon in a fluid that has high sodium concentration , why does the duration of action potential decrease compared to a control experiment in low sodium bath but maintained at the same osmotic pressure with choline chloride? Why does the amplitude of action potential increase in the experimental set ?

In short-  In the experiment, when the neurons are bathed in low sodium fluid but constant osmotic pressure, amplitude of action potential decreased, but duration of action potential increased.
I wanted to validate this with Nernst equation and/or GHK equation .
The increase is action potential amplitude with high extracellular sodium ( more sodium influx,more depolarization ? ) is intuitive?
But again I am confused because the membrane is only slightly permeable to sodium such that increases in extracellular sodium won't really alter the membrane potential enough to generate an action potential.
Also how does the action potential duration decrease in high sodium ?
What should be done if I want to increase duration of action potential while keeping the axons in high sodium bath ?

The duration of action potential is not the time to reach threshold voltage. It is the overall time the membrane stays depolarized.
In other words, why are the axons slowly repolarized when bathed in low sodium concentration(and also maintained at constant osmotic pressure with choline chloride ) compared to high sodium bath axons that are rapidly repolarized ?

How do you think the answer would've changed if choline chloride was not used ?

Could you elaborate: why does the duration of the ap increases? Due to a prolonged depolarization, or prolonged repolarization, or both, or due to another phenomenon? Doe you have a picture of normal and abonormal ap?

Duration of action potential,typically, can increase due to delayed repolarization and/or prolonged depolarization. I am confused about the part with the constant osmotic pressure, in the experiment that is somehow decreasing action potential duration. The concepts aren't clear to me fully. Referring to Hodgkin Huxley paper will help.

So is this homework or actual experimental data you are describing? In the latter case a picture would help as it would be very helpful to see the changes visually

It's not a homework question per se. This was an interview question to me . No figures were given. The above experiment was outlined and I was asked to predict the changes on duration and amplitude of action potential compared to the control.

High sodium extracellularly means an increased sodium concentration gradient across the membrane. This means there is a larger driving force for sodium to enter the cell once the sodium channels open at the start of the action potential, and hence a larger depolarization takes place increasing the action potential amplitude. The enhanced depolarization leads to an increased proportion of activated voltage-operated potassium channels that open upon depolarization. When more potassium channels open, more potassium will exit the cell, thereby repolarizing the cell to a larger extent, in turn stopping the depolarization step of the action potential faster. In all, the action potential develops quicker, as the depolarization is increased as well as the repolarization step, and hence the time it takes to execute an action potential is diminished.
Your subquestion as to the small sodium conductance is not valid, as during an action potential it is actually very high.
To increase the action potential duration you can increase the re-polarization step by increasing the extracellular potassium concentration, thereby diminishing the potassium concentration gradient and prolonging the repolarization step.

"In all, the action potential develops quicker, as the depolarization is increased as well as the repolarization step, and hence the time it takes to execute an action potential is diminished. " The duration of action potential is not the time to reach threshold voltage. It is the overall time the membrane stays depolarized. In other words, why are the axons slowly repolarized when bathed in low sodium concentration(and also maintained at constant osmotic pressure with choline chloride ) compared to high sodium bath axons that are rapidly repolarized ?

I have edited the question to  make the choline chloride part clearer.

I understand the meaning of the question and have answered it as far as I am aware. The choline keeps the potential constant so that sodium can be increased while keeping the membrane potential constant. Repolarization is slow in low sodium because depolarization is slow. Repolarization is initiated by potassium channels that are activated by depolarization as indicated in my answer. I am not talking about thresholds anywhere.

Or do you mean to say that frequency of action potentials increases when extracellular sodium concentration is increased such that duration of a single action potential decreases ?  Correct me if I'm wrong.

"To increase the action potential duration you can increase the re-polarization step by decreasing the extracellular potassium concentration." Action potential duration is increased by decreasing repolarization right ? So in this case by increasing extracellular potassium, so that potassium concentration gradient is decreased/abolished.

How do you think the answer would've changed if choline chloride was not used ?

This one occurred to me only now. I've edited the question again, in the hope of more answers.

The question is getting pretty broad. Nernst/Goldman equation will answer your added question.

Not different from @ChrisStronks answer. Just in different words.
Just for everyone's knowledge — you are referring to the Voltage-clamp experiment.
Situation 1: Sodium is depleted in the ECF.
Despite the fact that Na+ conductance is much less than that of K+ and the equilibrium membrane potential (hyperpolarized) is closer to Nernst potential of K+, absence of Na+ would move the equilibrium potential closer to the K+ Nernst potential. This would result in increase in the response time of action potential (AP).
Situation 2: Sodium is increased in the ECF
The consequence of this would depend on how much is the concentration of Na+. You can calculate the changed Nerst potential of Na+ using the Nernst-Plank equation.  How would it decrease the response time of AP?
It would increase Nernst potential of Na+ causing an increase in the sodium current. This would increase the rate of AP and therefore decrease the response time.

authors: Борат Сагдиев


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How do I import FASTA files into Haploview?
I'm trying to produce a haplotype network and so have decided to use the software haploview. However I'm having some problems importing my sequences into the software.
I Have my sequences in a FASTA format but I can't find a way to convert this into a format that haploview accepts.
Does anyone have any ideas how I can get from a FASTA format file (e.g. >Az01|Female|Azores AGGATCT...) to a phased haplotype format (Az01    Azores    0    4    2    2)?

You should let us know how your fasta files are like. What is your reference etc? These are the reads or assembled genomes?

@Luigi Collapser would just collapse redundant reads to a single sequence.

Shoot, I linked to the wrong tool!

What are your sequences? PED format is for SNP data, but I suspect you have a single gene.

I'm rather new to bioinformatics, so please excuse me if I'm a bit slow. They are reads of the ITS region of a shark species, and they're 910 bps long. I did produce a haplotype diagram in TCS, but I was told haploview was better. I'm looking at haplotypes from different geographic regions.

@WillPerry You can try this: Align reads → Get BAM → Get VCF (with GATK or something similar) → Convert to PED (VCFtools). There should be a better way; I am not aware of it.

@WYSIWYG Thanks, I've converted the aligned reads to a BAM file but when trying to produce the VCF file I was asked for a reference file. Do you know what this reference file is meant to be comprised of? I'm using PGDSpider with samtools and bcftools extensions.

@WYSIWYG Also, when I opened the BAM file in notepad it was unreadable; "‹     ÿ BC ÚUÖÍnÓ@ÅqW,ÀH¼Jå{çÎ... etc". Is this normal?

Yes you would need a reference. Your reads also have to be mapped to the genome first, to generate the BAM, so that you know the positions where the reads align. Reference is fasta file for the genome. BAM is binary; it won't be readable. You can use samtools to read it. For more info on VCF see here

@WillPerry When I read your previous comment carefully I realized that you actually need not use haploview. You can try this: Collapse redundant reads (while keeping a count) → do multiple sequence alignment. I am suggesting this because you are interested in just one region. You don't need haploview and all.


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Is there a rule for the annotation of the basepair or gene locus origin in bacterial genomes?
Since all bacteria have one circular chromosome, there is no designated origin to start the systematic gene locus numbering. Therefore, what is the rule to start the numbering at a particular point (i.e. why is in the E.coli K12 strain the thrL gene given the ordered locus number b0001? If the answer is: It is the first Gene downstream of basepair-1, then why is basepair-1 at this particular position)
Why the question? Since bacteria show frequently functional synteny between genes, should I be surprised to find a gene frequently associated with the (arbitrary?) annotation origin? If the annotation origin is i.e. the origin of replication that would be an interesting case of synteny, but if no such rule exists, then such a case would most likely just reflect the historic sequence of Genome Sequencing

I don't know this from experience, but since every bacterial chromosome has an origin of replication, it'd make sense to start from there

Even I think it is the ori. But let me find a reference

Trying to find a reference has me googling ridiculous things like "numbering base pair convention circular chromosome bacteria"

I guess it is not ori.. From E.coli genome GTF: NC_007779.1 RefSeq region 3710706 3710937 . - . ID=id233;Dbxref=GeneID:12934266;Note=ECK3735:JWS0001:b4489~origin of replication;gbkey=rep_origin;gene=oriC

I suspect it's based on some kind of linkage map generated by interrupted mating experiments a long time ago. It certainly makes sense that ThrL would be one of the first genes since it used in threonine biosynthesis, making it a good marker. Why they chose that marker could be arbitrary, possibly it happened to be downstream of the F factor integration site in whatever strain the original researchers where using. If I find some kind of literature about it, I'll post an answer.

We already discussed a similar question here

@har-wradim I am not sure if people use the same terminology these days (with genomics so popular). It would make sense to set ori at 0.

@canadianer: thrL is the first gene is the Ecoli reference sequence (pos 190) but I don't understand why it would make sense to keep it first in the order for all bacteria.

@WYSIWYG: In E.coli the old "point 0 min" corresponds to the currently accepted boundary between the last and the first bp's: see here a superposition of the two systems and these articles: "old" and  "new". I have the feeling, that for new bacteria point "0" is normally defined by ori.

[I'm sure we have a skilled microbiologist somewhere here, so he would correct my answer.]
The necessity to designate gene locations in classical bacterial model species predated the genomic era, so traditional maps were normally neither bound to origin of replication, nor were they necessarily expressed in base-pairs. In E. coli, for example the traditional map was created based on the F-pili-mediated DNA transfer experiments.
When whole genome sequences became available it was only natural to continue the traditionally defined numeration in terms of placing the "base-pair one". Thus, in E. coli "the traditional and physical maps ... linkage map are closely correlated".
My understanding of the current situation with bacteria without genetic prehistory is that their genomes are numerated either respective to classic closely-related species (if any) or according to the presumed location of ori. Just to give an example of how the dilemma was solved for the Buchnera genome: it was "assumed the DnaA box upstream of the gidA gene is the replication origin" and the authors decided to designate "the start of the DnaA box as base pair one".
As you see, still, even if the authors try to define "base-pair one" based on the position of ori, the problem is that this point depends on the ori-searching tool one uses and on the contemporary understanding of how ori-sites look like (direct determination of origins of replications are in many cases not easy). See e.g. this table with a revision of ori locations in a set of genomes: while most of the genomes received their numeration irrespective of ori, some of them were indeed bound to it, but the new analysis showed that these locations were inaccurate.


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Specialist evaluation for people aged under 40 years with stage 1 hypertension
Reading the NICE clinical guideline for Hypertension it says...

For people aged under 40 years with stage 1 hypertension and no evidence of target organ damage, cardiovascular disease, renal disease or diabetes, consider seeking specialist evaluation of secondary causes of hypertension and a more detailed assessment of potential target organ damage.

However it is not clear in the guidelines exactly what "specialist evaluation of secondary causes of hypertension and a more detailed assessment of potential target organ damage" would entail.
I understand that it is typical to carry out blood tests to look at kidney function, thyroid function, cholesterol and glucose levels; and that further tests such as a 12-lead ECG, echocardiography and renal ultrasound scan may be ordered if necessary to test for organ damage.
My question is what further tests would be performed by a specialist on a patient aged under 40 years with stage 1 hypertension and no evidence of target organ damage, cardiovascular disease, renal disease or diabetes? I have done several searches on Google but most of the papers I've read relate to patients who already have signs of organ damage or existing disease.

Alongside full guidance released by NICE they also produce treatment pathways which give further advice - here is the treatment pathway for hypertension.  You've listed most of the investigations that would be considered in your original question.
Investigations that may be considered as appropriate include:

Urine dipping for proteinuria or haematuria indicative of renal damage
Measuring of plasma urea and electrolytes and estimation of glomerular filtration rate, again as an indicator of renal damage
Measuring of plasma glucose, total cholesterol and LDL/HDL cholesterol to rule out additional risk factors as part of cardiovascular risk assessment - e.g. diabetes, hypercholestrolaemia
Fundoscopy to examine the retina for damage resulting from hypertension
12 lead ECG to show any changes compatible with left ventricular hypertrophy
Scanning for the presence of a phaeochromocytoma if clinically suspected

You may also find the professional reference page on hypertension from patient.co.uk useful.


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Can the eye distinguish between pure and composite colours and how do we measure this?
Red light plus green light makes yellow light.
Suppose I shone a pure red light, say 650nm, onto the same spot as a pure green light, say 550nm. The eye sees this two-peak spectrum as yellow.
This presumably means we are tricking the eye, since a pure yellow light source would also be perceived as yellow.
Do the cells on our retina treat composite spectra equivalently to corresponding single-peak spectra? If not, how do we quantify the gap?

I don't think it is perhaps quite right to think of light and light perception in this way, you are trying to make two continuous variables in to discrete groupings

Yes, we do perceive a composite spectrum in a way which is analogous to how we perceive the corresponding single-peak spectrum. Human beings have trichromatic vision, meaning that there are 3 types of specialized cells in our eyes for seeing color. Each one has a different color of light which produces peak stimulus, although they all perceive a range of colors:

(the axes are wavelength and normalized response)
None of the color-sensing cells has a peak color of yellow. In order to perceive something as being yellow it either has to be pure yellow or stimulate the 3 types of color sensing cells in a very similar way as pure yellow would. However, if you took very careful readings of the output signals from the color sensing cells you might see some subtle differences in the exact waveforms of the responses.

What tel explained is correct. I wanted to add that we actually see pure light in a composite way too.
Note for example that the M receptor has a peak at around 550nm, and a symmetric response curve. So, if you shine a 540nm light, the response of the M cone is the same as the response at 560nm. So, how do we know that it's a cool, bluish green and not a warm, yellowish green? By the response of the other cones. The ganglion cells in the retina combine the response of several cones to represent the wavelength of the light perceived by the photoreceptors (as well as some other attributes of the image within their receptive field).
As for "tricking" the eye, we're doing it all the time. Higher levels of visual processing will interpret colors depending on everything else perceived in the picture, such as light intensity, texture, and even cultural knowledge about colors. A mostly unbiased representation of wavelengths is only present at very early stages of visual processing.


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Coniferous trees in temperare rain forests
In temperate rainforest, the dominant plant form is often coniferous trees (source). However, coniferous trees are also the dominant plant form in a very different climate and form a different biome (boreal forest). Why are broad leaved evergreen trees not so adapted in temperate rain forests as in tropical rainforests? What is the advantage of needle-shaped leaves in the climate with temperate rainforest?

The Wikipedia article you link to notes that temperate rainforests may be either broadleaf or coniferous.

Yes, some parts are dominated by broadleaved evergreen trees, and some parts are dominated by coniferous trees.

The largest area of temperate rain forest in the world is on the west coast of North America, which has a summer dry season. In other words, at precisely what would be the best time for plants to grow (based on temperature), there's a shortage of water. (Summer vacation visitors to the rain forests on the Olympic Peninsula are often wondering "where's the rain?")
Conifers have small, waxy, and (generally, with a few exceptions) evergreen leaves. All the conifers in the rain forests of western North America are evergreen; that allows them to grow in the cooler months of the year, when there can occasionally be hard frosts (and when deciduous trees are dormant). The waxy, small leaves help them conserve water in the dry summers. A double advantage.
North of about central BC, there's no longer the summer dry season, but by that point the growing season is getting short enough that conifers have an advantage despite the perhumid climate (Prince Rupert, BC is further north than Edmonton, Alberta).
I'll add that this is not the only non-boreal climate where conifers are abundant: consider for example the piñon-juniper woodlands of the American Southwest or the Piney Woods of the Deep South.


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Can anyone identify this chrysalis? (Identified)
It's about 5 or 6 cm long. It's on the outside (north facing) wall of my garage about a metre above ground level.
Photo taken in Thailand near Hua Hin (about 12N 100E) in December 2014.

What a great find! :D Fantastic chrysalis. Thanks for sharing.

I've found it - it's a Common Rose Swallowtail (Pachliopta aristolochiae)
A few images on this page.
http://flickrhivemind.net/Tags/aristolochiae,butterfly/Interesting including these two

There is a picture also at http://en.wikipedia.org/wiki/Pachliopta_aristolochiae but this one is upside down compared to mine.

Mystery solved.


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Why do humans hear better between 2kHz and 5kHz?
I've recently seen the following image:

Source: https://commons.wikimedia.org/wiki/File:Hoerflaeche.svg
Translation (from German):

The upper boundary (Schmerzgrenze) is where it starts to hurt
"Musikwahrnehmbarkeit" is where you can hear music
"Sprachwahrnehmbarkeit" is where you can recognize speech
"Hörschwelle" is absolute threshold of hearing (ATH)

While the ATH seems to be relatively smooth, there is a noticeable "gap" between 2kHz and 5kHz. Does anybody know why this is the case?
Some possible explanations I've heard are:

Evolution: Hearing a baby cry
Evolution: Hearing leafs rustling
Coincidence: There is no good reason for that.

The image is from wikipedia commons and has no references. It might be wrong. Do you know similar graphs? Do you eventually have this kind of information for other animals?

The main reason is this is the area where harmonics in human speech are most prominent.

Acoustically, we hear better in the 2-5 kHz range because our auditory canal resonates in that range (specifically, around 3 kHz). Our ear looks something like this (U Miami):

The auditory canal is part of the outer ear, which amplifies sound so that it can be converted into electrochemical signals by the middle and inner ear. We hear better in the 2-5 kHz range because the resonant frequency of the auditory canal is in that range.
The mechanical question of "how does this work" is usually easier to answer than the "why did this evolve?" question. Since reproductive fitness is the driving force of evolution, hearing babies crying (between 1-5 kHz) is the best guess I can come up with.

Do you think the resonant frequency could be different without severely influencing other properties how we hear / what we hear? Is this different for other animals with similar ears?

Changing the resonant frequency wouldn't change what we hear but would change the threshold at which we hear different things. I don't actually know about other animals, perhaps ask another question if you want more information?

This doesn't really answer OP's question, it only gives the mechanics behind it, and almost puts effect before cause. The reason the auditory canal is tuned to that frequency range is because our voices' harmonics are most prominent in that range.

You may never see this, but I also had this question - I think this may be a fun take.
The 2-5kHz range is associated with the third and fourth formants of the human voice, and these formants are used primarily in singing.1 After reading some discussion about possible evolutionary reasons that humans sing - It seems that sexual selection could have played a role2,driving improvements in perception of that frequency range.
Also, as mentioned earlier in this thread - the ear's resonant frequency is most sensitive around 3khz, which correlates nicely to the f3, f4 frequency range.

"... our auditory canal resonates in that range (specifically, around 3 kHz)." - Luigi

Finally, I'll link a neat video 3 in which a primatologist explains a phenomena in which female gorillas sing to emanate comfort/safety. Could possibly have a related function in humans.
p.s. please excuse the 3rd source :)
1^ Frequency range of human singing formants f3,f4
2^ A thread discussing the evolution of singing
3^ Gorillas singing analysis

This is exactly why, except that it's not just for singing. Human speech itself has a lot of energy in these bands.  We're most sensitive in this region because it helps us to hear each other speak better. A lot of voice CODECS specifically oversample this region as a result.

@stix on the other hand, why didn’t the human speech/voice cord evolve to be in a different frequency band?

@kal The average human trachea is around 11cm. The wavelength of 3 kHz is around 11 cm. That band is the resonant frequency of the average human vocal tract. It's due to the size our bodies evolved to be.

@stix thanks for verifying/clarifying :)

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


text:
Can dolphins actually communicate linguistically?
Humans use "language." By language, I mean the thing I am using right now to talk to you.
I know dolphins and orcas have very complex communication systems and also seem to process linguistic and gestural commands.
But do they have their own languages? Where is the evidence for or against? If we take two group of dolphins Group A and Group B, would Group A speak one language and Group B speak another?

We don't know. They are certainly very good at learning our languages, but we don't know if they have their own in the wild. This isn't really an answer (I don't have enough reputation to post this as a comment) , but this article may help.

I heard that they have different languages/dialects, problem is rather if one could consider them complicated enough

As a matter of fact, orcas too are dolphins!

Dolphins and orcas do have dialects. Of course there are species specific dialects and it has been shown that orcas reared with bottlenose dolphins tend to learn the latter's dialect. Dolphins of the same species also seem to have regional dialects, as mentioned in this BBC post (I personally do not trust in non-research articles much, but nonetheless in this case the article indicates a certain possibility of a phenomenon). However, this page also reports the same finding and this source seems to be much more reliable. There are citations too that are at present inaccessible to me. Both the sources say that bottlenose dolphins from Shannon estuary in Ireland, "speak" different dialect compared to those from Cardigan Bay in Wales.
The actual research work is this:

Hickey, R. (2005) Comparison of whistle repertoire and characteristics between Cardigan Bay and the Shannon estuary
  populations of Bottlenose dolphins (Tursiops truncatus) with
  implications for passive and active survey techniques. School of
  Biological Sciences, University of Wales, Bangor

Apart from having regional dialects, the cetacean communication also seems to have other features of a "language". I am pasting excerpts from this article which basically reports a study on the acoustic communication or codas in sperm whales. This may apply to dolphins as well.

Individuals within social units have preferred associates among
  members (Gero et al. 2008), indicating differences in the way an
  individual interacts with other members of its unit. These preferred
  associations among unit members suggest the possibility of an
  individual discrimination system.

.... most adult animals within a social unit shared the most common coda
  types, with the exception of the mother-calf pair whose repertoires
  were different from those of other unit members and each other. Apart
  from the mother-calf differences, the repertoire similarities of other
  members did not support the hypothesis of individually distinctive
  coda type repertoires. This sharing of coda repertoires suggests that
  they allow group membership recognition, at either the unit or clan
  levels. This hypothesis is further supported by the fact that social
  units seem to form groups preferentially with other units of their own
  clan (Rendell & Whitehead 2003b).

To be able to learn human sign language (remember Flipper?), their brains are certainly hard-wired for complex communication.
I once read a paper that showed a whale repeating the same song almost exactly. The song was one and a half hour long. Couldn't find it now, but I found some nice articles showing the complexity, consistency and evolution of whale songs. They also show that different populations have different songs (languages or dialects, if you prefer), and that these songs evolve through the years.
Orcas and dolphins are members of the Odontoceti, while whales are Mysticeti. I don't know if the verbal communication of the first group is as elaborated as that of the second, but I don't discard this hypothesis.
Whale Song Explained - great work of art using colored symbols to illustrate the different patterns of sound that make up whale songs.
Songs of Humpback Whales
Large Scale Changes over 19 Years in Songs of Humpback Whales in Bermuda
Dynamic Horizontal Cultural Transmission of Humpback Whale Song at the Ocean Basin Scale


text:
What is the name of this plant (see pic)?
This plant was found growing in Colombia.

@j.musser is probably a good person to ask... also consider instead asking on the gardening stack exchange

@GriffinEvo Thank you, I guess I'd agree with Luigi on Lupinus :)

Better suited to [gardening.se]?

That looks like a member of genus Lupinus, flowering plants native to North and South America:

I couldn't find a good resource for species of Lupinus in Columbia so I can't help you with the species, unfortunately.

Thank you! It's size confused me a little: it's much bigger compared to the ones I've seen in Europe, and it has smaller flowers.


text:
Are domesticated animals really "more intelligent," or is that a myth/misunderstanding?
Often do I hear people speaking of how the domestic house cats are more friendly, less ferocious, less savage-like, and smarter and/or than their distinct but equivalent feline-species friends, like lions, tigers, jaguars, panthers, leopards, cheetahs, etc. Is this provably true in any form or way?
Are domesticated animals really "smarter" or less ferocious, or are some simply, but assumption of lessened threat potential, more so inclined to deem the house cat/dog as less ferocious simply because it's not such a big threat? Look at it this way:

This little beast here is "very cute" because he/she is small and barely 9 lbs. When playing, he/she isn't directly threatening to many human's safety, and many people are not afraid of cats; however, is he/she really smarter because he/she is safer and less dangerous to us humans only?

This beast, however, is hundreds of pounds heavier and many feet longer. Is it considered more savage-like because it can seriously harm and possibly kill humans by playing a little rough, which is like how a 9 lb. house cat would play equivalently, but would give you some light scratches at worst.
I've also heard arguments about "friendliness" of felines, usually claiming that house cats are friendlier due to evolution and nurturing/upbringing; lions/tigers, on the other hand, are claimed to be naturally unfriendly and have "more wild" in the, and incapable of being as "friendly" or "trustworthy" as a house cat. Point is, I'm probably not the only person who's heard this. Also, consider other animals, like dogs.
Dogs come from the grey wolf, to put it simply. Compare both a typical house dog and a wild grey wolf, and it's pretty obvious that many would assume the house dog is safer, friendlier, and less harmful, despite the fact that some domesticated dog breeds can pack a greater bite than the wild grey wolf.
Comparing the house dog's behavior to the wild grey wolf is also not a good measure of "friendliness", as compare a savage Homo sapiens from an uncivilized territory to a common city person, and you'd think the same thing: that the savage human is "less intelligent" and the city person is more so.

Not sure what are you asking exactly, but the term "more evolved" makes no sense in evolutionary biology. All extant species are equally evolved.

Generally, "more evolved" would be synonymous with "more intelligent" to those not so familiar with the evolutionary process, as some people might think that evolving means growing better, smarter, or more "advanced" (comparing to modern humans as a reference), such as in fictional Pokemon series.

I'm not sure as to what you are asking, but during breeding of domesticated animals, ferocious and dangerous specimens were probably less likely to be used to make a next generation (of cats, dogs etc). Hence, timidness was a favorable characteristic I think. The tiger you are depicting is not domesticated like the dog for example. Way more controlled-bred generations of puppies have preceded a present-day dachshund than captive tiger-kittens have preceded this tiger on the picture. Hence, the timidness factor is way more pronounced in truly domesticated animals.

I am not sure about this but I guess aggression is inversely correlated with intelligence.

And as @MarchHo said there is no term called more evolved. I replaced the term with more intelligent to that your question remains on topic.

The question is indeed badly formulated, but I think there is an interpretation which is very interesting, even though probably not exactly what the OP wanted to ask. If we measure "intelligence" in animals by observing traits common in intelligent humans, such as speed of learning new tasks, or ability to understand a message they receive, do domestic animals have more of these traits than their wild cousins? Did humans manage to select for animals who learn better, or did wild animals evolve better learning? I'd be glad to see a well referenced answer along these lines.

Domestication has little, if anything, to do with intelligence.  From biologist Jared Diamond, the 6 criteria for domestication are as follows:

Flexible diet – Creatures that are willing to consume a wide variety of food sources and can live off less cumulative food from the food pyramid (such as corn or wheat), particularly food that is not utilized by humans (such as grass and forage) are less expensive to keep in captivity. Carnivores by definition feed primarily or only on flesh, which requires the expenditure of many animals, though they may exploit sources of meat not utilized by humans, such as scraps and vermin.
Reasonably fast growth rate – Fast maturity rate compared to the human life span allows breeding intervention and makes the animal useful within an acceptable duration of caretaking. Some large animals require many years before they reach a useful size.
Ability to be bred in captivity – Creatures that are reluctant to breed when kept in captivity do not produce useful offspring, and instead are limited to capture in their wild state. Creatures such as the panda, antelope and giant forest hog are territorial when breeding and cannot be maintained in crowded enclosures in captivity.
Pleasant disposition – Large creatures that are aggressive toward humans are dangerous to keep in captivity. The African buffalo has an unpredictable nature and is highly dangerous to humans; similarly, although the American bison is raised in enclosed ranges in the Western United States, it is much too dangerous to be regarded as truly domesticated. Although similar to the domesticated pig in many ways, Africa's warthog and bushpig are also dangerous in captivity.
Temperament which makes it unlikely to panic – A creature with a nervous disposition is difficult to keep in captivity as it may attempt to flee whenever startled. The gazelle is very flighty and it has a powerful leap that allows it to escape an enclosed pen. Some animals, such as the domestic sheep, still have a strong tendency to panic when their flight zone is encroached upon. However, most sheep also show a flocking instinct, whereby they stay close together when pressed. Livestock with such an instinct may be herded by people and dogs.
Modifiable social hierarchy – Social creatures whose herds occupy overlapping ranges and recognize a hierarchy of dominance can be raised to recognize a human as the pack leader.

From his Pulitzer prize-winning book.
We (as a species) domesticated animals (and plants) by selecting traits we sought, and then breeding to keep alive/emphasize these traits. In hunting animals (retrievers, for example), intelligence may be one of those traits. Others might include obedience, speed, agility, even dark-colored coats for camouflage.
It's not really correct to say "more evolved" as @MarchHo explains in his comment. Rather, you might say "more docile", or "less aggressive".
Keep in mind that less aggressive, domesticated animals are not necessarily more intelligent than their wild counterparts.
status-myth

After working with goats I suspect that intelligence was actively selected against.

@user137 interesting point, I hadn't thought of that

Please read my comment to March Ho's; it has quotes for a reason.

@TinselDancer that's exactly why I emphasized the way I did, to show people who don't know otherwise that greater intelligence ≠ more evolved ≠ more advanced

It's not entirely clear what you're asking.  If you're asking whether domestic animals are more friendly to humans than wild animals, the answer is generally yes.  However, this does not make them "more evolved".  Domestic and wild animals are ultimately derived from a shared common ancestor, so they have been evolving for an equal period of time.  In general, domesticated animals have been selectively bred for traits that make them useful or appealing to humans, so it is to be expected that they possess more of these traits than their wild relatives.
An interesting detail is that, in addition to behavioral traits like increased tameness, many domestic animals tend to display certain physical traits such as floppy ears, shorter faces, and coloration differences, which were not present in their wild ancestors.  A recent article has proposed that these traits are the result of mild developmental defects which have been selected for by the process of domestication.  A long-running experiment on domesticating silver foxes has lent some evidence to this idea.
By the way, comparing cats to tigers is not really a meaningful comparison.  The closest wild relative to the housecat is the wildcat, Felis silvestris, which looks like this:

Interesting thoughts. Inbred albino rats (e.g. Wistar rats) are considered to be timid, while the pigmented rats (e.g., Long-Evans) are more aggressive. The latter are not (or less) inbred, and can be considered to be less domesticated, I guess

"More intelligent" as more capable of learning
Domesticated varieties of animals generally aren't "smarter" as per objective measurements of brain power, however, I'd argue that they would feel smarter for us because they have different patterns of learning.
For most living beings, there is a general shift of the "explore vs exploit" behavior balance as the individual ages - juvenile individuals observe and absorb new behaviors, often by imitating their parents and siblings, while adult individuals tend to lock in the behaviors they already have instead of exploring new options.
Humans differ from other animals in that this "juvenile" behavior lasts much longer, and the same applies for many domesticated animals - a mid-age dog in many behavioral aspects is more similar to a wolf cub than a wolf of the same age. Such an animal would be more capable and willing to learn new patterns of interaction and tricks than a similar wild animal, and thus feel "more intelligent" to a human observer - while it's an entirely different difference.
Also, as far as I understand, this doesn't neccessarily apply to all domesticated animals which we raise for food and resources, but to 'companion' animals like cats, dogs and horses.

Please provide some references

It could be original research, @Jay.

May be, but what if it were not ? Its our right to ask references, if you have any doubts about your rights you can always feel free to use the helpcentre


text:
Will gene mutations give rise to a protein that is shorter than the full length protein?
What is the relationship between deletion or insertion of nucleotide in the gene sequence and the protein's length that is coded out from the mutated gene?

It depends on the nature of the insertion or deletion.
Many mutations are point mutations, where one single nucleotide is changed:
ATGACTACGCTATTCAGT
M  T  T  L  F  S

ATGTCTACGCTATTCAGT
M  S  T  L  F  S

Notice that changing the fourth A to a T caused a T->S change in the final protein, and didn't change its length. However, an insertion/deletion is different. Starting with this sequence:
ATGTCTATTGACGCTATTCAG
M  S  I  D  A  I  Q

Let's have an insertion, an A after the A in position 7:
ATGTCTAATTGACGCTATTCAG
M  S  N  STOP

Notice we now have a stop codon (TGA). This means the protein will be truncated, and will be much smaller. That isn't always the case. Rather than adding an A at position 7, let's add it after position 9:
ATGTCTATTAGACGCTATTCA
M  S  I  R  R  Y  S

The protein is about the same length, but the AAs are completely different than the original version after the insertion:
M  S  I  D  A  I  Q
M  S  I  R  R  Y  S

This is called a frameshift mutation. Biologically, these mutations are harmful because they change all the amino acids after the mutation, the protein is often not functional and can end up being different sizes (if a stop codon is now in frame or out of frame) and the protein can even end up being unstable and rapidly degraded.
So, to answer your question about the length of the protein, it'll increase/decrease by one AA every time 3 nucleotides are added/removed, but can increase or decrease drastically if a stop codon is added or removed by a frameshift mutation.


text:
Why should a tumor look like a crab?

Origin of the word "cancer"
The disease was first called cancer by Greek physician Hippocrates (460-370 BC). He is considered the “Father of Medicine”. Hippocrates used the terms carcinos and carcinoma to describe non-ulcer forming and ulcer-forming tumors. In Greek this means a crab. The description was names after the crab because the finger-like spreading projections from a cancer called to mind the shape of a crab. – source

So the cancer cells spread in a way that tumor looks like a crab. Why? Why doesn't it, for example, have a potato-like spread in which cancer cells form a sphere?

I'd guess that the projections are supportive vasculature. Also keep in mind that tumours don't actually really look anything like crabs. The Greeks seem to have been quite imaginative (see constellations).

Potatoes aren't very invasive - that is, they can't crawl where they don't belong, they can't spread between tissues, etc. I'm very sure this is why they weren't described as potato-like. Also, the picture you have is a scanning electron microscopic image. This is not what the Greeks saw. They probably were describing an invasive tissue with projections and vascularization.

Oh, the pic is only a simulation of what Greeks saw, I just wanted it to be there to stop some "users" from asking: What do you mean by crab? :-)

+1 for vasculature. I don't know this definitively but it makes a lot of sense

It's also worth pointing out that potatoes are from South America and were not introduced to the old world until the 16th century (source). Even if the tumor did look like a potato, Hippocrates simply wouldn't have had the vocabulary to describe it as such.

The term is mostly symbolic and tumours were compared to crabs perhaps because they are tenacious like crabs. This was what I read somewhere long time back. This site has some discussion on the etymology of cancer (disease).

Such projections are more formally known as spiculations. Most commonly, we talk about spiculations with respect to the radiographic appearance of malignant breast and lung lesions. This paper* describes the correlation between the mammorgraphic appearance of spiculated breast lesions and their pathology (microscopic appearance), which is a reasonable start at addressing the "why" question you pose. The authors define spiculations as follows:

A spiculated breast lesion is defined as a mass or an architectural distortion characterized by thin lines radiating from its margins.

Here is a picture taken from that paper which shows the mammographic appearance on the left and the microscopic appearance on the right, with the arrows pointing to the spiculations.

The linked paper gives many other examples of the microscopic and radiographic analysis of such tumors. It also explains that the two primary reasons for the spiculated shape are:

desmoplastic response
tumor infiltration (which occurs along anatomic ductal structures)

According to this report, the first explanation is more common. To understand the why behind the shape, we need to know the mechanism of this desmoplastic response. As described in the linked Wikipedia article, desmoplasia is not actually the tumor itself but dense fibrous tissue that is induced with malignant tumors invade healthy tissue. The mechanism of this is not entirely clear, but the Wikipedia article sets forth two theories:

The reactive stroma hypothesis postulates that tumor cells cause the proliferation of fibroblasts and subsequent secretion of collagen that acts as a scaffold. This scaffold apparently forms the outline of the "crablegs".
The tumor-induced stromal change hypothesis states that tumor cells themselves differentiate into fibroblasts and secrete the collagen that forms the spiculated scaffold.

*Franquet T, De Miguel C, Cozcolluela R, Donoso L. Radiographics. Spiculated lesions of the breast: mammographic-pathologic correlation. 1993 Jul;13(4):841-52.

"Cancer" is so named because the cancers Hippocrates first observed looked like crabs to him. If he had first observed cancers that most resembled potatoes, cancer probably would have been named differently today.

Cancerous growths reminded Hippocrates of a moving crab, which led to
  the terms carcinoma (malignant tumor) and cancer (ulcerated malignant
  tumor).

Reference http://onlinelibrary.wiley.com/doi/10.1002/cncr.25553/full
My point is, there is no "need" for a tumor to look like a crab or any other particular shape. Most tumors are probably irregular in shape. Most often they just look like lumps. I think breast cancer turns out to look like a crab fairly often (not sure why) and it was precisely breast cancer that Hippocrates was studying, probably because it's fairly close to the surface of the body, and, hence, fairly accessible and easy to observe. That's not irrelevant when there are no proper surgical techniques and anaesthetics.

Why is this downvoted?

I didn't downvote, but this answer doesn't seem to significantly answer the question.

Yeah, looks like I wasn't paying much attention and misunderstood the question. :)


text:
Blood type frequency given probability
I have calculated the probability that any child will have a particular blood type from both the genotype level and the phenotype level assuming the human ABO Rh system is followed.
Here are the genotype probabilities:
AA+/+ 49/1764
AA+/- 98/1764
AA-/- 49/1764
AO+/+ 98/1764
AO+/- 196/1764
AO-/- 98/1764
BB+/+ 49/1764
BB+/- 98/1764
BB-/- 49/1764
BO+/+ 98/1764
BO+/- 196/1764
BO-/- 98/1764
AB+/+ 98/1764
AB+/- 196/1764
AB-/- 98/1764
OO+/+ 49/1764
OO+/- 98/1764
OO-/- 49/1764

Here are the phenotype probabilities:
A+ 441/1764
A- 147/1764
B+ 441/1764
B- 147/1764
AB+ 294/1764
AB- 98/1764
O+ 147/1764
O- 49/1764

Here is the frequency of the blood types in the 1st generation by genotype:
AA+/+ 5/101
AA+/- 5/101
AA-/- 5/101
BB+/+ 5/101
BB+/- 5/101
BB-/- 5/101
AB+/+ 5/101
AB+/- 10/101
AB-/- 5/101
OO+/+ 5/101
OO+/- 5/101
OO-/- 5/101
AO+/- 10/101
AO+/+ 5/101
AO-/- 5/101
BO+/+ 4/101
BO+/- 4/101
BO-/- 4/101

Here are the numbers and their genders; a number represents an individual from a population of 101:

Male:
0,2,5,10,11,17,20,22,23,31,34,40,41,44,46,47,50,55,59,61,62,68,71,79,80,82,85,88,89,92,94,100

Hermaphroditic(and fertile):
4,8,16,25,32,64
all the rest are female
M/F mating: 11,904 offspring in 2nd generation H/A mating(hermaphrodites can mate with other hermaphrodites, males, females, and even themselves): 3636 offspring in 2nd generation
If you divide these by 6 you will get the amount per operation. The operations I am taking into consideration are +, -, *, /, ^, nth root, and arrow arrow(tetration).
So how can I take the frequency of blood types at the genotype level, probability of blood type at genotype and phenotype levels, and total number of offspring to get a 1st order estimate of the frequency of these blood types in the 2nd generation?

This question is very hard to read, I suggest that if you put some effort in to the formatting you'll more likely get a good answer :)

"Here are the numbers and their genders:" ... what do you mean here?

Since this biological data is from my Math World story numbers such as 0 and 100 have genders. Their gender is determined by 4 sex chromosomes. XXXX = female, XXXY = male, XXYY = hermaphroditic, and XYYY = male

So you mean there is 32(?) males, 6 hermaphrodites, and 101-(32+6) females??

yes that is what I mean

*"The operations I am taking into consideration are +, -, , /, ^, nth root, and arrow arrow(tetration).": This part is also unclear

In math world the eggs and sperm have these operational chromosomes. For arithmetic they are +, -, *, /, ^,nth root, and arrow arrow(tetration). Different combinations of egg and first sperm to fertilize it lead to different operations done with the numerical value of the mother and the father. The mother is always the first addend, first factor, dividend, minuend, base, index, or is an exponent and a base in the case of tetration(which is repeated exponentiation).


text:
Evolutionary chronology - if any, which species have evolved in the last 100 years
I heared somewhere, I cannot remember where, that there has not been an evolution observed in our lifetime. In life science class, right at the start, we was doing the usual MRSGREN (how to tell if something is a living organism), and the tutor said that you can also tell something is a living organism if it evolves. So I asked if there has been an observed evolution in our lifetime. She said that there had been many but could not recite any off the top of her head, so the next week she handed me a piece of paper with 8 or so websites that aparrently corroborated her claim. I have not got the paper anymore but I recall there been on there the peppered moth or something. So I set out to look for a chronological list of evolution but could not find an authoritative one. I could only find something on wikipedia that indicated that species have been dying out for the past thousand years, but nothing saying that any have evolved.

Many, many viruses.

Evolution is a continuous process, there's things that have evolved since you asked this question. I think you are looking for speciation events (what you called an "observed evolution" - this would be a very incorrect term)

@Peteris That is what I am talking about. I cannot find anything to say that the species x used to be species y over the last 100 years due to a random mutation. And does anybody think that the examples of the peppered moth changing colour due to industrial pollution, as shown by Bernard Kettlewell, constitutes as a new species? Could it not just be that there is a biochemical malformation which is due to the pollution rather than it being because of a random mutation? - OP
PS, I know my terminology is not too great, but answers of all levels will be appriciated.

Every single species in existence has "evolved" over the past 100 years. Evolution is a constant process. You are asking whether we can observe evolutionary change in a given species over a short time span, not whether evolution is occurring. I know this sounds like pedantry but it is a very important distinction.
That said, yes, of course we've seen evolution in action in short time spans. The classic example is the various bacterial species that have developed resistance to antibiotics. As very nicely illustrated by Garry Trudeau:

If you want more rigorous evidence than a comic strip, have a look at Wikipedia's page on antibiotic resistance or read Demerec, 1948(1).
Another example is described by Yona et al.(2) who show that subjecting yeast to high temperatures (heat stress) for a few generations causes genetic changes that help the cells deal with the stress. This is, clearly, evolution in action. In fact, they even show that the first response is the duplication of an entire chromosome (think of it as a crude, bludgeon-like solution) which is later suppressed by other, more subtle, compensatory mechanisms which arise to replace it.

Demerec, Milisav, "Origin of bacterial resistance to antibiotics." Journal of bacteriology 56(1), 1948
Yona et al., "Chromosomal duplication is a transient evolutionary solution to stress", PNAS, 109(51), 2012.

Of course, these two references are just two random examples among thousands of examples. Would be good to also include a reference of observed changes in gene frequencies observed in nature, eventually among the human population if we can show for example how the sickle-cell/malaria gene evolve in response to pathogen within the past 100 years.

Antibiotic resistance - as antibiotics itself - are evolutionary very old processes. These have not developed in the last 100 years. See for example here.

@Chris well, yes and no. I am not suggesting that all resistance to antibiotics happened over the last 100 years, simply that some have which means they can serve as an answer to the OP. There is a huge wealth of evidence that the widespread use of antibiotics has resulted in the development of resistant strains. Of course some such strains already existed but do you deny that others have arisen recently as a direct result of human medical practices?

As Peteris claimed, we cannot witness the complete evolution of a specie in our life time. Our life, being a frozen moment in the eternal journey of evolution, not always gives us the pleasure to completely understand the process of evolution(also the purposes). But we can witness some minute details, which we can consider as the sub sets of a complete evolution. By evolution, most people think of the complete development from one specie to another, but this kind of evolution to develop a completely different specie will take a millions of years. So we could conclude that those kind of evolutions cannot be witnessed in our life time.
But there are those evolutions which are more dramatic and came into existence within a period of some decades, so considering these minor evolutions(or we can call it variations) we have a couple of cases were some species develop,

Resistance over chemicals(pesticides,insecticides)
Adaptions to withstand predations
Cope with available resources(veg/non veg diets)

1. Resistance over chemicals(pesticides,insecticides)

Reappearence of tougher bedbugs that are harder to kill
Entomologist Dini Miller of Virginia Tech says bedbugs probably developed thicker, denser, waxlike exoskeletons, also called cuticles, that repel chemicals in pesticides. To test the hypothesis, her group is comparing cuticle-coding genes in both insecticide-resistant and susceptible bedbugs, as well as measuring their cuticle thickness and hydrocarbon content, which indicates how much wax is present.
  Reference
Evolution of Microgadus tomcod
  After General Electric dumped polychlorinated biphenyls (PCBs) in the Hudson River from 1947 through 1976, tomcod living in the river were found to have evolved an increased resistance to the compound's toxic effects.1 Scientists identified the genetic mutation that conferred the resistance, and found that the mutated form was present in 99 percent of the tomcods in the river, compared to fewer than 10 percent of the tomcods from other waters.
  Reference

2. Adaptions to withstand predations

Lizards are Evolving to be Dancers
Take the southeast fence lizard, for example. When fire ants were accidentally introduced to the States about 70 years ago, the fence lizard found itself defenseless against them. The ants had no natural enemies, and it only took 12 of them to take a lizard down in about a minute. Seventy years later, the lizards that live closest to the port where the ants were first introduced have evolved an unlikely strategy for dealing with their antagonists. How unlikely? Well, there's a dance involved, which makes these animals the first on record to employ the West Side Story method of self-defense.
While other lizards respond to ant attacks by "sitting still, just hoping the ants would go away," these smooth operators developed an ant-shaking shimmy that they've passed on to their kids. And those kids have longer legs for quicker get-aways. Just so we're clear: Nature, not weird daddy issues, has created leggy lizards that thwart attackers through shaking what their mommas gave them.
  Reference

3. Cope with available resources(veg/non veg diets)

Lizards are Rewiring Their Own Guts, Right Now
  In 1971, scientists introduced 10 Italian wall lizards to an island in Croatia, but right after they dropped them off, the Croatian War for Independence prevented the researchers from following up on their little lizard guinea pigs. In fact, the scientists couldn't get back to the island until 2004. When they did, they found 5,000 lizard descendants who had not only annihilated the entire indigenous lizard population, but also rewired the shape of their own innards to accommodate the local diet.
Before their introduction to the island, the wall lizards were carnivores, so their digestive systems weren't built for leaf-eating. But on an island short on insects and long on plants, a strictly carnivorous stomach would be a one-way ticket to Deadville. So the lizards developed things called cecal valves, which were muscles that slowed down the process of food digestion and gave them more time to break down plant cellulose. But growing new gut muscles wasn't all the lizards had up their sleeves. They also grew bigger heads for stronger bites, and dropped territorial defenses.
  Reference

Evolution is an aggregation of all these combined traits and mostly evolution is accelerated when the species are geographically separated, time is a crucial factor  with evolution. We are unlucky to witness a complete evolution in our neighborhood, but all these accumulating traits which change a specie to adapt with a diverse environment is a powerful evidence towards evolution and its working.

Other examples: nylon-eating bacteria and aerobic citrate usage in E. coli in the long-running experiment by Lenski et al..

Short generation cycles
By definition, we shouldn't expect to observe within our lifetimes the evolution of any species with a generational cycle comparable to our lifetime (mammals and such) since species differentiation requires a multitude of generations.
The directly observed evolution thus is limited to short lived organisms such as bacteria, viruses, plants or insects, with an emphasis on the first two.
It is possible to directly observe evolution in an experimental laboratory setting by taking a strain of bacteria that doesn't possess a certain capability (e.g. resistance to some chemical compound), periodically introducing this compound and accelerating the mutation rate by e.g.  radiation, observing the formation of a new species of bacteria that is able to resist this chemical.

Drastic changes in allele frequency due to differential survivorship can be observed within a single generation. There are examples of important change in allele frequency in human due to disease prevalence (adaptive changes) and bottlenecks (non-adaptive changes).

I think this is opinion based and wrong, as @remi.b notes, I am sure examples of very modern evolution could be found in human

@Remi.b Changes in allele frequency within a population by themselves would not constitute formation of a new species, for that you need to observe creation of a new, different population with traits that didn't exist before. The evolutionary changes that have happened in homo sapiens during the last couple millenia definitely don't constitute evolution of a new species.


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Potential to destroy viruses using prions?
Could a prion be used to sufficiently deform a viral protein in order to make the virus it is a part of incapable of reproducing? For example, take the common cold's VP1 protein and turn it into a prion, then inject that prion into someone with a cold. Would this prion ever come into contact with the virus? Would it actually deform the virus? Can we make prions?

Issues I see with this idea is that finding a protein that misfolds the VP1 protein in a reliable way would be hard, and getting those proteins to specific cell types to fight the virus would be hard.

I think you are making many questions together that are independent (e.g. can we make a prion and whether it would be in contact with a virus). The context is too broad. Why don't you try focusing on some question one at a time?

Prions are misfolded "versions" of proteins already present in the genome. These tend to bind to their properly folded counterparts and catalyze their misfolding into prions. Although unlikely, it is not impossible to imagine that they might interact with other macromolecules. That being said, injecting a human with prionic particles for any reason (especially in a clinical trial for the common cold) is EXTREMELY unlikely. Even if you prove that it works in animal models, injecting a person would be considered too risky. Additionally, the "benefit" of that would be marginal - curing the common cold, from which > 99% of people recover even without any medication. Given that there is great risk and very little benefit, we will most likely never know for sure how feasible this is (at least for the common cold). As a concept, it could work, but would be extremely difficult to get right.

Now I'm confused. What is the difference between binding with a protein in your body and one in a virus? And why would it be risky? Don't prions only affect their protein? This would also work on Ebola, HIV, and any other viral disease.


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How is DNA Read
Little odd question here. I was told that DNA was read in groups of three.
Assuming this, my question is: Which way would better describe how the DNA is read.
(123)456789 to 123(456)789 to 123456(789)
or
(123)456789 to 1(234)56789 to 12(345)6789
Assuming that the string of numbers 123456789 represents a DNA sequence.

first hit on google: http://learn.genetics.utah.edu/content/molecules/dnacodes/

DNA codes for proteins via codons. A codon is a combination of three nucleotides. As there are 4 different nucleotides available in DNA, there are 64 permutations possible. These 64 codons code for the 20 amino acids and 3 stop codons. Hence, many amino acids are coded by several different codons - the genetic code is said to be redundant.
Typically DNA sequences have a single reading frame (but see @user3790338's answer for an interesting exception to this rule). The reading frame is, basically, defined by the first amino acid of the protein that it decodes. Thereafter, each subsequent triplet is one codon, in a non-overlapping way (123 - 456 - 789 - etc.). Note that DNA sequences contain so-called introns that intervene the coding DNA. These regions are eliminated post-transcriptionally. For clarity-sake I have disregarded them in my answer.
However, one has to realize that this coding of DNA is only important phsyiologically during translation, i.e., when mRNA is being translated into a protein. It is the ribosome that actually reads the codons and stop codons to determines which amino acid is to be incorporated in the growing protein and when to stop translation. Hence, although we read DNA sequences in terms of codons, the cellular machinery doesn't read DNA, it reads mRNA.

Perhaps I misunderstand what you're saying, but stop codons do not terminate transcription.

Not to be pedantic, I also just noticed that you said introns are eliminated post-translationally, which is not true.

"It is the ribosome that actually reads the codons" -- I'd expect the DNA -> mRNA transcription  process  to do that as well, if only to figure out when to stop transcribing the DNA.

@Jan-Dvorak Transcription doesn't involve codons and its termination is by another mechanism. It occurs down stream of the CDS.

Assuming the first coding position is 1, the DNA will be read as: (123)456789 to 123(456)789 to 123456(789). There are fairly few exceptions to this, e.g. some viruses (e.g. http://www.ncbi.nlm.nih.gov/pubmed/1966841), where reading frames overlap like in your second example. This is because the viral genome is much smaller and needs to code all of its proteins into as little nucleic acid as possible. Note that there is more than one way for frames to overlap.


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Can someone help me analyze this article?
I need to read this article — "Beyond the rainbow" by
Marie-Claire Koschowitz et al., for an exam.
Following are some questions for which I could not figure the answer out after reading.
1) Why does this miniaturization necessitates insulation ? Following is quote from article: "For fast-growing, presumably warm- blooded animals , such miniaturization would only have been possible with sufficient body insulation. "
2) Dinosaurs suppose to have tetrachromacy. The article mentions "dinosaurs were endowed with the highly differentiated color vision of birds". Does this mean Dinosaur's "inherited" their tetrachromacy from birds ? Why does the article mention reptiles before that ? Are birds reptiles ?
3) The article starts talking about how mammals develop fur and lost their highly differentiated color vision because they gave up structural color signaling. What is the direct connection between mammals and the dinosaurs ? I don't see the parallel here....why bring the mammals into the discussion ?
4) What is the connection between pennaceous feather and planar feathers ?
Any or all questions answered is welcome ! Thanks !

You cannot ask for an explanation of an article. A) It would be too broad B) Homework questions are considered off-topic unless you show an effort. It is fine to ask something that you do not understand from a paper but that has to be a precise point. And the article is in clear and understandable english.

could you provide an actual link?

@shigeta Link provided

I do not think it realistic to expect anyone can explain an entire paper here. If you have a particular question, that is, if you do not understand a particular sentence, or small paragraph (that is, something concise) you may try to ask that.

@WYSIWYG I have updated the question to reflect effort and understanding. Please unmark it from "hold" so that I may receive some answers.

I think the question, although still broad (i.e., multiple questions) is eligible for re-opening. I have adapted my answer.

you guys are too tough on newbies - asking for clearer question should be first resort. closing second.

@JennaMaiz If you can then please ask some points as a new question. For example the vision part can be separated from the feather/fur part. Miniaturization can also be another question and there are some posts here related to that topic already; you may also have a look at those. I am voting for reopen but it would be nice if you narrow the question down.

Agree with @WYSIWYG. Also voting to reopen but there are probably too many different questions.

@WYSIWYG  What are the guidelines for asking a question like this ?(Can I even ask something like this ?) Moderators on this site are way too strict closing the question immediately and asking to show effort, reword, edit the question. I understand they have a job to keep this site clean-but all the same, my impression was this kind of site is not a good place to get a rapid response(like before a final as was my case). Anyways, if necessary, you can delete the question if it doesn't fit this sites guidelines.

@JennaMaiz: did you get a useful answer in time for your test? I admit some questions are shot at too quickly at times. I tried to do my best answering it, and we have re-opened the question for you, despite the fact that the question was, admittedly, too broad. We all do our best :) Good luck in the future and please don't hold back asking more questions. This question was very interesting and the article you linked was of notable quality and I loved reading it.

@shigeta I do think we should be a bit more friendly towards newbies, but don't necessarity find it hostile to close a question if the reason is communicated clearly and in a nice manner. In this case, the question is really broad, and it is asking several separate questions that should be posted separately. There are cases where several subquestions for a single paper/issue are suitable (e.g. clarifying several methodological steps). However, in this case, the subquestions are unconnected and they sometimes seem to deal with tangential statements in the paper (so dependent on other papers).

@shigeta Oops, sorry for reviving a really old discussion - didn't notice the timestamp.

I will answer the questions one by one-

Why does this miniaturization necessitates insulation ?
An organism's volume determines the total amount of heat that can be stored. The loss (exchange) of heat between the body and external environment mainly occurs on the skin's surface. Hence, body volume determines how much heat is stored, while body surface determines how fast that heat is dissipated to the environment. Volume increases with a power of three with radius, while surface increases with a power of two. Hence, smaller animals have large surface-to-volume ratios, which decreases rapidly with body size. Hence, small animals will dissipate relatively more heat per unit of time.
Dinosaurs suppose to have tetrachromacy. The article mentions "dinosaurs were endowed with the highly differentiated color vision of birds". Does this mean Dinosaur's "inherited" their tetrachromacy from birds ?
No, birds are the closest living relatives to dinosaurs, and birds can be said to have inherited tetrachromacy from dinosaurs - see the cladogram below.

Why does the article mention reptiles before that ? Are birds reptiles ?
Birds are not reptiles, they are separate classes within the animal kingdom.
What is the direct connection between mammals and the dinosaurs ? ... why bring the mammals into the discussion ?
Here below is another cladogram; there is no obvious, direct (evolutionary) connection between dinosaurs and mammals. The thing is that dinosaurs ruled the world before the last mass extinction, thereafter it were the mammals. That's why the authors discuss them both, I guess. Especially since we are mammals it may make sense to draw parallels.

What is the connection between pennaceous feather and planar feathers
As far as I could track the two down, they are the same (Prum, 2006)

Lastly, in response to your original question, before edits: Here is a link with a plain-English popular-scientific web article published online by the first author.


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What is difference between breed, variant, subspecies and species?
What is the difference between breed, variant, sub-species and species? Are there any similarities between sub-species and sub-population of a region?

what do you mean by "Are there any similarities between sub-species and sub-population of a region?"?

You may want to add the term strain in you list. @WYSIWYG I would guess that the OP asked between sub-species and sub-population of a region because (s)he has some understanding that species is a term that applies to taxonomy while population is a concept that is used to define a collection of individuals that reproduce and live over a geographical region.

A species is commonly defined as the largest group within which interbreeding produces viable offspring.
A sub-species is a subgroup below the level of a species.  One definition is a group which can interbreed successfully with other subspecies, but does not do so in practice (e.g. due to geographical isolation).  Other terms like variety, form, etc., may be used in some domains to indicate various groupings below the species level.
A breed usually refers to a population of a domestic animal that has been selectively bred for specific characteristics.
A population is a set of individuals within a species that live in the same geographical region.  Depending on rates of gene flow, different populations within a species may eventually differentiate into subspecies or distinct species — this is known as allopatric speciation.

So is there any difference in meaning between population and subspecies? Note that while you are giving the most commonly used definition of species, those definition only apply to lineages that reproduce sexually. I would love to have the definition of the word strain as well in this list. I would tend to think that many of these concepts are poorly defined and are used with different definitions in different field of biology.

@Remi.b These concepts are indeed loosely defined and the accepted definitions vary across different subdomains (e.g. microbiology vs botany vs zoology); this is just an overview.  As for population versus subspecies, population just refers to the members of a taxon in a given region, with no implication of a distinct genetic lineage.

As Remi said, what is strain actually?


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Double use of ATP in relaxing myosin & active transportation of calcium?
Is the ATP molecule which is bound to the myosin head for relaxation of the muscle (i.e., to break the cross bridge) also utilized for active transport of calcium to the sarcoplasmic reticulum during muscle relaxation?

ATP is used for ion pumps as well as movement of molecular motors. It is of course not the same molecule that does both simultaneously. How can it!!

Thanks. ..I just read in a book , I got confused. ..thanks for clearing up the matter

@WYSIWYG: you have my deepest respect for understanding this question! I edited accordingly, thanks! Convert to an answer and you will get a much deserved +1

Yeah I somewhat guessed the meaning. Tried some edits but I left it to the OP to explain the rest.

ATP is used (hydrolyzed) by ion pumps to transport ions such as calcium against their concentration gradient.
Molecular motors (such as myosin and kinesin) also couple ATP hydrolysis with movement.
However both these processes are separate and just because calcium flux changes happen during muscle contraction doesn't mean that it is the same ATP that drives some kind of a bifuntional enzyme to perform both tasks.
Moreover calcium is released during the contraction phase from the sarcoplasmic reticulum (SR); pumping back the calcium to the SR happens during the repolarization (there is no myosin movement at this stage).


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Why are some vegetables/fruits seasonal?
How does the mango tree perceive the summer season, so tree starts producing the fruits?
Every tree requires sunlight to grow but what limits the production of fruits to a certain season?
For example: Mango only grows in summer season, whereas banana grows in all seasons.

Many plants start flowering (and subsequent seed / fruit production) based on light, temperature, and / or humidity changes, which tell them summer is near. That is when they need to grow fruit. Surely, there are plants trying to look for sunlight, pollinators, good conditions for seedlings, in the winter, but they are specially adapted, and thrive in their niche only through some season sensing similar to the summer-flowering plants.
At the Equator there isn't much difference between seasons and days, and there  should be no need for such mechanism. Bananas are suited to the Equator, meaning banana trees don't know what seasons are.
Plants in temperate climates care about seasons a lot. We put them in greenhouses and we play with their light, in order to force off-season flowering. Tomatoes are kept in the greenhouse not because we don't like them shivering outside, but because we want to fool their temperature-sensing organs that summer is here.
At the Tropics there is an important difference in the amount of rain water and a smaller change in day duration. Mangoes are more suited to the Tropics, meaning they care about seasons. People who grow mangoes in greenhouses try to fool them by adjusting humidity, but I couldn't find any evidence that it is humidity rather than day length.


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Why does our voice change when we get affected by cold or cough?
Why does our voice change when we get affected by cold or cough? I observed the voice change thing in so many people including me.

What has the picture of the virus got to do with your question?

You observed a virus?

If I didn't upload the pic, then I can't able to post my question, because of "this question does meet quality standard" red color box. But I posted relevant pic to my question.

The picture is irrelevant, and once again (this must be the 5th time I've told you specifically) stop using block quotations - learn how to use this site properly!

When we get affected by cold or cough, the virus infects in the upper respiratory tract and prevents you from making smooth vocal sounds.

Your vocal cords may be covered with mucus or affected by swollen surrounding tissue during infections of the upper respiratory system.

The important point is that your voice is influenced by airflow, and your vocal cords. When we're sick, and it depends on what it is, a number of factors change the sound of your voice by influencing the two of these, either: By changing airflow due to respiratory tract swelling or fluid buildup, or by damage/swelling/alterations to the vocal cords. In a couple  of examples: A weak airflow might produce a higher pitch or weaker voice, or perhaps swollen vocal cords produce that hoarseness associated with decreased frequency of vibration.


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How are lesions in the RNA corrected?
I quite understand why thymine is present in DNA. So we can mark it out where cytosine undergoes a reaction and is converted to uracil. Then we can repair the DNA.
But how can we make that out in RNA ??

Note that the nucleobase is thymine not thiamine. Thiamine is vitamin-B1 and is a cofactor for certain enzymes. I corrected it and this is just for your information.

Actually very good question.

RNA is shortlived and need not undergo repair. A "mutated" RNA will degrade and will be replaced by the correct RNA.
Even though RNAs are shortlived compared to DNA (which does not really undergo turnover), some RNAs are stable and have low turnover. Nonetheless RNA would be present in multiple copies it is improbable that all of them would have undergone mutation.
Moreover RNA with certain mutated codons e.g. non-sense mutations are cleared off by the exosome.
Thanks to har-wradim for pointing out about RNA repair mechanisms. There are few reports that say that methylations in the RNA can be corrected by the enzymes AlkB (in E.coli) and its eukaryotic homologue hABH3. These enzymes were known to repair methyl lesions in the DNA (1-methyladenine and 3-methylcytosine), but it was subsequently shown that they can act on RNA as well [1,2].
However there seems to be no mechanism for repairing deamination damage; this study has demonstrated an artificially designed system which is capable of targeted RNA deamination (but there is no system yet that can fix a deaminated base in RNA).
This article comments that AlkB is tightly regulated because if uncontrolled it can demethylate functional methylations too. Overexpression of AlkB is actually toxic to the cells unless they are under alkylation stress by agents such as EMS/MMS (Ethyl/Methyl MethaneSulphonate).
But IMO RNA repair is not as essential as DNA repair because of aforementioned reasons.

RNA repair does exist: http://www.ncbi.nlm.nih.gov/pubmed/18289040

@har-wradim Was not aware of that. Let me see; it seems to be only in the case of alkylation

+1, of some relevance here is also the fact that there are proofreading mechanisms acting during transcription: http://www.sciencedirect.com/science/article/pii/S0959440X09001626

I forget the reference, but mRNA is also checked during the first round of translation, after the ribosome reads the mRNA the first time the proteins bound the mRNA are changed to mark it as okay, if the ribosome fails to successfully a protein the mRNA is marked for destruction.

@user137 perhaps you are referring to NMD and nonstop-decay

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