How to measure growth of algae with colorimeter I am doing an lab for IB Bio and don't know how to use a colorimeter to measure growth in algae. The experiment I am doing will measure the effect of pH on algae growth. The algae will be taken from a fish tank and will include cyanobacteria, diatoms, and algae bloom. I don't know how the transmittance/absorption will relate to growth. I also don't know which wavelength of light to use. Help would be appreciated, thanks!

Let's be clear, you are using a colorimeter, not a spectrophotometer?

Can you provide the brand name and model number of this colorimeter?

Have you learned about the Beer-Lambert Law? It states that A = Ecl where

A is the Absorbance

E is the molar extinction coefficient

c is the concentration of the unknown

l is the length of the light path through the sample (the standard path length is 1 cm in spectrophotometers).

The first thing you need to do is measure lambda Max, the wavelength of light that is absorbed the most (or transmitted the least) by your sample. The Beer-Lambert law is linear when A is between approx. 0.1 and 1.0.

So take a dilute solution of the algae and starting at the smallest wave length of light that the device can emit (you can vary the wavelength?). Take readings of the Absorbance and then increase the wavelength by 10 nm. Starting at deep purple, and ending at far red, write down the A values. Plot this data with A on the Y-Axis and wavelength in nm on the X-axis. There should be a distinct maxima in the curve, that is the most sensitive wavelength, and is the one you should use for all your experiments. If the algae is green, then the maxima should be over in the red end of the spectrum (like chlorophyll).

Next you need to make a standard curve that correlates the Absorbance at lambda max with the number of algal cells in the cuvette (the test tube you put in the colorimeter). That means you need an independent method of counting the number of algal cells. If they were bacteria or yeast then you could plate them on agar-filled Petri dishes and count the number of cells per mL (for example). For some cells if you have a high powered microscope and a hemocytometer then you could visually count the number of cells per mL. If neither of these methods are available then you could measure the mass of algal cells by weighing them on a balance.

So by some method you will be able to plot the number of cells in the broth vs. the Absorbance (plot A on the Y-axis).

From this you can empirically determine the molar extinction coefficient of these algal cells.  Then you just need to measure the Absorbance at lambda max on  dilute aliquot of the cell culture and you will have an accurate measurement of the number of cells per mL.

With this assay working then you can inoculate a bunch of identical cultures, that vary by the pH of the growth medium. By removing small aliquots of the cultures at the same time points you will be able to plot the number of cells (on the Y-axis) versus the time they have been growing, and you will see if varying the pH alters the shape or magnitude of these growth curves.


Shouldn't evolution have taken care of baldness already? It is my understanding that the hair on the head is there to protect us from sunburn.  I've never seen a bald animal, so isn't evolution in charge of addressing these type of things?

How is it that evolution gave us a thumb, but hasn't found a way to keep the hair on our heads?

As is typical for questions about fitness, this question has more than one valid answer.

The essential question @AndrewSalmon is answering is the right one:

"If evolution eliminates disadvantages, why can xyz trait still be seen the population?"

Here is a more complete list,

1) The trait is not eliminated by evolution since it is manifested after reproduction.  The classic example of this sort of trait is senescence.  Why do we grow old and die?  Clearly it doesn't stop us from having offspring.  I generally don't find this sort of answer informative. Its not a bad argument for the traits of bipolar and schitzophrenic tendencies which can manifest as a chronic mental condition, often in the 30s after many people have children.
These traits are fairly common (1 in 6) in the population.
It is usually arguable that these traits are of some sort of advantage from some perspective (including my examples).  In this case @Andrew argues this.  I'm not sure I agree, but you can read his post for the argument.

2) Pleiotropy. The idea that the negative trait evidences more than one trait.  In this case one might say that baldness is tied with another trait that is beneficial.  Some say that the cause of male pattern baldness, which is an excess of testosterone, would be tied in with other masculine signals, which can often outweigh disadvantages of being bald and trying to find a mate.  A trait like baldness could also for instance be tied to a desirable trait in women, causing it to persist in men as a result of the advantage of say, less hairy women.  I probably wouldn't take this stand either, though its conceivable.

3) "Neutral variant" The third explanation that I will put out is that baldness simply isn't a trait with enough disadvantage (if any) that it should be removed from the gene pool.  While there is evidence that baldness is a disadvantage come friday night, to say that a trait is disadvantageous we have to see, in the long run - over the lifetime - really is a disadvantage.  I think I would agree with those who say that while some women do not find bald men attractive, its not enough to stop them from having kids, which is all evolution cares about.

And if you happen to be balding probably what you should care about, guys!

If evolution should eliminate male baldness, then why not eliminate sterility, homeliness, impotence, poverty, obesity, being dull, living with your parents and adolescent awkwardness?  These are probably even more important obstacles to finding a mate? All of these traits are beneficial traits that are maladapted to modern life or genetic accidents.  Evolution can't get rid of them at all I think.

For an even more complete discussion of the general subject, see Dawkin's "The Extended Phenotype".  Baldness is not discussed however.


Is there such thing as a generic "metabolic type"? A while ago I picked up a book called "Eat right for your metabolic type". The book discussed the effects of the endocrine system on the overall shape and the speed of metabolism.

The book outlined few major metabolic types:

Adrenal
Thyroid (hypo/hyper)
Muscular

The book proceeded to discuss the overall shape of the body, including shape of fingers to help identify the metabolic type and give suggestions on which foods to avoid for a particular type.

The book then gave examples of effects of foods on metabolic types - for example an Adrenal type who eats too much sugar would crash and compensate for this by sleeping.

Since I can no longer find that book in print, I'm interested if there's really such a thing as a metabolic type that can be easily identified ? Are there indeed some foods that people should avoid eating?

That book was likely crap, but in short the answer is yes, probably there is a genetic basis in the metabolism, with human 'types' that could benefit from a personalized nutrition. The discipline studying these relationship is called nutrigenomics, and the main concept is similar to what is being told for personalized medicine. The bad news is that unfortunately this is not easy to identify, surely not from the form of your finger.


Regional circulation and Cardiac output? I am reading my study materials and think what is the systemic POV here

  Regional circulation Blood flow within the tissue/organs based on the functional demands of the tissue.
      E.g. The blood flow to the brain should remain relatively constant from a systemic POV (13% of CO at rest).

What is the POV here?

Extension to the question and explanation.
The last part is just 13% of maximal cardiac output.

It might be as simple as 'point of view'.


Mutated Sperm - What happens? I saw on TV that not all sperm are the same. Some have mutations like 2 and 3 tails?  There were other mutations as well.

If one of these mutated sperm actually fertilized an egg, would the embryo be mutated in some form or fashion?

Yes, the embryo would get that DNA mutation.

Both sperm and egg are haploid, meaning they only have 1 copy of each gene. When the sperm fertilizes the egg, the resulting child is a diploid, meaning he/she has two copies of each gene. However, if the sperm was mutated, then child has one mutated copy of some gene(s).

Depending on the gene(s) that are mutated and the sequence of the mutated gene(s), this could result in non existent to severe consequences.


Unknown aquatic larvae These critters have taken up residence in standing water in a small terrarium. It is home to several frogs and lizards. If they will coexist peacefully, I have no objection. If they will harm plants or critters I'll have to evict them.

Those are collembolans. The common name is "springtail". Several groups of collembola are semi-aquatic. They are not larvae, but adults. There is a nice paper on aquatic collembolans here: https://link.springer.com/chapter/10.1007/978-1-4020-8259-7_36


Using RNA-seq to compare gene expression across patients instead of between Control and Experimental conditions I am working with RNA-seq data from the Cancer Genome Atlas TCGA and I have been reading about how people have compared gene expression levels measured by RNA-seq. Many of the papers I have read talk about "differential expression" for comparing each gene's expression levels in the Experimental and Control conditions.

In TCGA data, I typically have a patient cohort who have had the mRNA in their tumors sequenced just once so there is no Experimental-vs-Control dynamic. I am interested in finding which patients' tumors show gene-expression that is significantly higher than the rest of the cohort but I have not had any luck finding literature describing this kind of comparison. I'm thinking maybe I can apply existing differential expression techniques to my situation but that seems cumbersome and not-necessarily appropriate so thought I'd ask the community here if there's a better way of finding which members of a cohort are outliers for specific genes.

Also: all of my RNA-seq data has already been RPKM normalized for me. I have been advised that using RSEM instead would be better for comparing gene expression across multiple samples but, for logistic reasons, I'm probably stuck with my RPKM-normalized expression levels.

Fundamentally, I'm looking for the best way to compare gene expression across samples to determine which samples have outlying high/low gene expression. Intuitively, I figure I could just compute median z-scores for each gene's expression levels within my cohort and consider anyone with a |z-score| greater than 2 to be an "outlier" but I haven't found any literature to support this kind of approach either.

Any suggestions, papers, or advice will be greatly appreciated.

When you say RPKM do you mean crude RPKM or the estimates that you get using expectation maximization methods like cufflinks and eXpress?

It is better if you get your RPKM or FPKM values from one of these programs because you can differentiate between transcript variants.

I have mostly used cufflinks and eXpress. Cufflinks package is better for multiple datasets. You can use cuffquant (which takes SAM/BAM) files to compute FPKM. Cuffquant will also need a reference GTF file. Cuffquant gives a binary .cxb file which you cannot read directly. Once you have generated the .cxb files for all your cohort samples, then pass all these files to cuffnorm. It will normalize the data and give you FPKM values for each gene in each sample in the form of a huge table.

Next point is which genes do you wish to compare. Do you want to compare known oncogenes which show consistent upregulation in all cancers? Actually there is a paper in which they have done this (I'll let you know the reference when I find it. Not able to recollect now).

You can then see how many of these genes show consistent expression in your cohort. Basically you need to identify a set of genes before you go on to study which patient shows anomalous expression.


What motivates birds to make birdsong? I was pondering the question "Why do humans make music?" and on an intuitive level, my answer was "because of the feelings it evokes of course!"

But I then wondered, what about songbirds? Does a songbird have a feeling that compels it to make songs? I know there are plenty of instances of birds dancing and singing (at least, some call it that), but what motives does a songbird have to make birdsong?  How does this compare to the emotions and motives humans feel?

Why do bird sing?

The main reason, male bird sing to attract mates (often, only males sing). Birds may also sing to communicate to their peers. For example a song can mean "This is my territory, you'd better not approach!". There are other reasons birds can sing (although I think I cited the two most important ones); you'll find much more information if you just google why do birds sing?, there are plenty of very accessible online articles on the subject. Here is one such article that you may like reading

Talking about emotions is always difficult due to the absence of a good definition of what an emotion is. But anyway... yes, if females are attracted to the mates that sing well, it probably (depending on your definition) means it cause them to feel some emotions (sexual excitement for example).

Evolution of music in birds and humans

Bird song to attract mate (sexual selection). Humans, on the other hand, have evolved music production for different reasons (or at least this is what we think). The field of evolutionary musicology is a field in the junction between evolutionary psychology and biomusicology. In evolutionary musicology (and in evolutionary psychology) empirical testing is very complicated and therefore, today we can only think and make hypotheses but we can't test them. So always take with a grain of salt what you read in those fields.


Is there any definition of complexity about gene and protein according their function? Sorry for such a question,if it is too naive.

Is there any definition of complexity about gene and protein according their function?If so,what is the relation between them?

Proteins and genes usually are classified in superfamilies and families acording with its inner structure (mainly its domain organization). Domains are parts of the protein with its own 3D structure that usually have their own function and acts more or less in an independent manner.

However, this doesn't talk very much about their complexity. Myoglobin and hemoglobin, for instance, are very related proteins and thus are classified in the same family. However, hemoglobin forms tetramers, while myoglobin is a single molecule. It's not unheard that very close-related proteins may differ in their association with other proteins, polymeration pattern, addition of new domains, etc. Very similar poteins may have very different functions, i.e. catalyzing similar reaction in opposite directions or in very different pathways, or acting in different parts of the cell or the organism.

In biology, it is desirable for any classification to be based in evolutionary criteria, since not only it is a more neutral and unbiased way to classify biological things, but also provide information about the origin and structure of those. You could classify proteins by their structure, number of motifs, number of domains, number of different domains, size, function (in fact, there is a very useful and widely used classification for enzymes), etc; and you could classify the genes according to its number of exons, structure of its promoter/enhancer, policystronic or not, etc. However, this classification will usually prove itself to be inferior to an evolutionary classification.


Why lipophilic molecules can pass phospholipid bilayer, in spite of 2 hydrophilic layers? It is commonly told that, hydrophobic/ lipophilic/ nonpolar molecules can quite easily pass phospholipid bilayer, and hydrophilic (polar or ionic) molecules can't pass (when no protein aid that); because hydrophobic nature of the lipid.

But in the same logic, hydrophobic molecules shouldn't pass through the bilayer. Because there are 2 hydrophilic layers in the membrane. i.e.

A and A' .

Then how the hydrophobic molecules can pass through A and A'?

I guess, it is due to thin diameter of A and A' . Is that?

Good question. This is my take.

It's not just the surface of the membrane that's polar. There is water (polar) on both sides of the membrane. In most animal cells there is also an unequal distribution of charges across the membrane. The environment outisde of the cell is typically positive due to an excess of positive ions, especially sodium. The inside of the cell is typically negative due to an excess of negative ions such as phosphate.

This means the hydrophobic molecules aren't any more at home in the environment outside, or inside, the membrane than they are at the surface. There's no reason to suppose any more repulsion at the surface. So, just due to their random kinetic motion they will find themselves at the membrane's surface, some with the necessary kinetic energy to cross.

There's another way to view this. We shouldn't think of the membrane as allowing hydrophobic substances to enter. We should think of it as NOT allowing hydrophyllic substance to enter without a proper ID check by proteins in the membrane.


The simplest organism that can learn? What is the simplest organism that was observed to learn: change its behavior permanently in response to some event/stimuli in a way that this change persists even if the event does not happen again?

I don't know if it is definitively the simplest, but the simplest organism with a nervous system that has been studied extensively is probably C. elegans, which is definitely able to learn.

Some basic learning abilities have also been shown in amoebae.

References:

Ardiel, E. L., & Rankin, C. H. (2010). An elegant mind: learning and
memory in Caenorhabditis elegans. Learning & Memory, 17(4), 191-201.
Saigusa, T., Tero, A., Nakagaki, T., & Kuramoto, Y. (2008). Amoebae
anticipate periodic events. Physical review letters, 100(1), 018101.


Evolution of endosymbionts? Mitochondria and plastids in eukaryotes evolved through a process of endosymbiosis. How does an event like a eukaryote engulfing a bacteria, become a part of the genome? Some of these primitive eukaryotes could have been more predisposed to more vigorous endocytosis as a result of their DNA, but how could the physical event account for evolution of organelles?

I think you mean mitochondria and chloroplasts and are referring to the endosymbiont theory (Reference to the unedited question as it was originally asked).

The definition of symbiosis for the most part tells you how coevolution can be accounted for by this theory.

The larger Eukaryotes provided the protomitochondria with a protected environment for growth and the protomitochondria produced usable nutrients for their hosts from molecules that the eukaryotes were unable to process on their own.

The two organisms struck up a balance and the mutually beneficial relationship allowed both to prosper. As the Eukaryotes with protomitochondria were better able to utilize more of the chemicals from their environment than those that did not play host to the protomitochondria, they had a survival advantage that other early Eukaryotes did not.

As plant cells have both mitochondria and chloroplasts, it is believed that one of the eukaryotes with a mitochondria endocytosed a photosynthetic prokaryote. This event wasn't as much of an advantage as the first symbiotic relationship. Since all eukaryotes have mitochondria or evidence of ancestors that had mitochondria, but not all have chloroplasts, then it was beneficial enough that the photosynthetic organisms were also able to coevolve within the eukaryotes and alongside the mitochondria, but they were not beneficial enough so as to give those cells that hosted chloroplasts enough of an advantage that they took over all life on Earth.

Mitochondria also have their own DNA, so their complete genome is not found in the eukaryotic genome. Over evolutionary time, mitochondria have lost the genes that allowed them to live freely, so you could not extract them from eukaryotic cells today and expect them to grow external to the eukaryotic cell. They require substances that the eukaryotic cell makes. Whether there was recombination between the two genomes or just that both had the same function at one point and then through genetic drift caused the mitochondria to lose the homologous gene, I could not say.


Phospholipid movement in cell membranes What causes phospholipids to flow so quickly in cell membranes? In Biology by Cambell et al. they state that a phospholipids can travel up to 2 micrometers per second. Is that a random movement or has anyone found that phospholipids have a current?

There must be charge considerations in the movement of molecules in the lipid membrane. There is also a consideration that some species of phospholipids will migrate to portions of the membrane with sharper or smoother curvature.

Waves of electrical potential can propagate along a lipid bilayer as well, which is very important to nerve axons and extended structures like that.

In general though the membrane is held together by vanDerWaals forces like other non-polar solvents.  As such, the movements of lipids and proteins and other amphipathic molecules in the membrane are still largely Brownian (random) in the 2D surface of the membrane.


Is this a roach or a beetle? I'm pretty sure it's a beetle due to the lines on it's back/rear but I'm not positive and if I'm wrong I need to take action quickly. Thanks in advance :)

This is a click beetle (Elateridae), so not a cockroach. This is most easily seen by the long pointed corners/angles at the posterior part of the pronotum, which is part of the “click” mechanism they use to flip themselves when they land of their back, or to startle predators.


Is APB an antagonist of the mGluR6 receptor? APB is a glutamate analogue specific to the mGluR6 receptor of ON retinal bipolar cells. It is used in research into receptive field processing by blocking the ON channel. Why is it not called an antagonist?

APB (2-Amino-4-phosphonobutyric acid) is a metabotropic glutamate receptor agonist, not an antagonist, and in many publications it is indeed referred to as an agonist, so I think your question is somewhat ill-posed. For example:

Yamashita, M., & Wassle, H. (1991). Responses of rod bipolar cells isolated from the rat retina to the glutamate agonist 2-amino-4-phosphonobutyric acid (APB). Journal of Neuroscience, 11(8), 2372-2382.

You can find many many more by searching "2-Amino-4-phosphonobutyric acid glutamate" on Google Scholar.

The reason that APB suppresses ON bipolar cells is because metabotropic glutamate receptors are often inhibitory rather than excitatory. Glutamate is typically thought of as excitatory because ionotropic glutamate receptors such as AMPA and NMDA receptors are non-specific cation channels that depolarize and therefore excite cells. Metabotropic glutamate receptors operate through g-protein second messenger cascades. In ON bipolar cells in particular, there are cation channels that are closed by mGluR6 activation, which therefore inhibits them.

Here's a review article that describes this as well as other basic information about bipolar cell function:

Euler, T., Haverkamp, S., Schubert, T., & Baden, T. (2014). Retinal bipolar cells: elementary building blocks of vision. Nature Reviews Neuroscience, 15(8), 507-519.


How To Avoid Macro-Evolution Confusion? I regularly encounter students who believe humans came from amoebas and when asked why they often say Macro-Evolution has been scientifically proven.

Macro-evolution is defined as evolution at or above the species level, which leads to the problem: Scientific evidence does exist for speciation at the Biological Species Concept (BSC) level, but not for all species concepts and only if a helpful definition is employed. Lions and tigers are considered different species and have been know to reproduce--sometimes with fertile offspring. Therefore, what benefits are there to such a broad category as macro-evolution?

The distinction between lions and tigers is so much smaller than feathered vs. scaled creatures! Surely the current definition of macro-evolution is overly broad and confusing to newcomers. Only the fuzzy edge of the macro-evolution definition has been proven. Proving that 1 inch of a yardstick exists does not prove that the rest does. There is a distinct lack of rigor to the statement that "macro-evolution has been scientifically proven."

Surely the definition of macro-evolution could be chopped in half with the goal of distinguishing between relatively trivial changes (Lion vs. Tiger, but beyond micro-evolution) and relatively non-trivial distinctions (either at and above the genus or the family level). The "trivial" changes could be termed "Middle Evolution" and work something like this:

1.) Middle evolution: evolution at or above the species level, but below the family level.

2.) Macro evolution: evolution at or above the family level.

Substitute the word genus for family in the above definitions if that seems better. I admit that line would be somewhat arbitrary, but would not the term "Middle Evolution" be informative?

The only place that the terms "macro-evolution" or "micro-evolution" are generally used, are in creationist rhetoric. They are not terms used by biologists. This is because there is no need to create distinct categories. In reality there is only "microevolution". Macro-evolution is not a different thing, merely an accumulation of many micro-evolutions.

  what benefits are there to such a broad category as macro-evolution?

None. Which is why such a term has been abandoned.


Why do the size of the phase 1 notch vary among cardiac cells? The size of the phase 1 notch varies among cardiac cells. It is prominent in myocytes in the
epicardial and midmyocardial regions of the left ventricular wall  and in ventricular Purkinje fibers. However, the notch is negligible in myocytes from the endocardial region of the left ventricle.
What's the reason?

Between at least the endocardial and epicardial regions, I believe the transient outward current is facilitated much more in epicardial cells. This article demonstrates the differences in Ito between the two cell types in dogs.

I'm also recommending the following article about Ito phenotypes: "Transient outward potassium current, ‘Ito’, phenotypes
in the mammalian left ventricle: underlying molecular,
cellular and biophysical mechanisms"


Are sizes of potatoes normally distributed? I'm currently researching the variability of sizes of potatoes when all of the potatoes in question have been harvested from a single field. One question keeps coming up in my statistical analyses: Under normal circumstances, are the sizes of potatoes - within a single field - normally distributed? (Please feel free to define the weasel words "normal circumstances" in the most helpful way you can imagine.)
Human height is often given as one of those classic examples of a normally distributed phenomenon. The little that I know about plant biology suggests that the central limit theorem applies just as much to potatoes as to the human body: the lengths of potato tubers and the lengths of human bones should have similarly-shaped distributions. But is that correct?

A bit of context to my original question: what I'm trying to do is to take the mean and standard deviation of my data and then, using the 68-95-99 rule, construct a series of confidence intervals, which I can then test or refine by looking at other data sets. Obviously, no real data set is going to conform perfectly to a model; I just need to know that, in principle, potato sizes are normally distributed enough that my method for drawing up confidence intervals isn't hopelessly misguided.

According to Evaluation of the Effect of Density on Potato Yield and Tuber Size Distribution potato tuber size was estimated using a normal distribution but they are not normally distributed
They found that a Weibull distribution with specific parameters estimated better than a normal distribution.
In fact you should not expect a normal distribution because there are no potatoes of negative size  As such you expect a gamma distribution.  The Weibull distribution is in the same family of distributions.
But in many cases the normal distribution is used since the probability of a negative number is negligigble.
Does this mean that potato sizes are still the result of many factors? It would seem so


What is the right definition of 'Sex Linkage'? I am confused about definition of "sex linkage". I have found different definitions but they do no match.

From P.S Verma, V.K Agarwal cell biology, genetics, molecular biology, evolution and ecology:

  If the genes are situated in the same chromosome and are fairly close to each other, they tend to be inherited together. This type of coexistence of two or more gene in the same chromosome is known as linkage.

From: Anthony J.F Griffith "Introduction to genetic analysis

  In general, genes in the differential regions are said to show inheritance patterns called sex linkage.

From: Wikipedia

  Sex linkage is phenotypic expression of an allele related to the allosome (sex chromosome) of the individual.

Linkage is the tendency of two genes present on the same chromosome to be inherited together. The degree of linkage depends on the distance between the two genes, i.e two genes that are physically close are less likely to be separated onto two different chromosomes during recombination/crossover.

So this is what your first definition trying to convey.

Sex linkage simply means that a gene is to be found on the differential region of a sex chromosome (and not an autosome). See it as (gene) Linked to sex chromosome.

Note: Linkage and sex linkage are not the same.

An Introduction to Genetic Analysis, 7th edition makes it a bit easier:

  Sex linkage is the location of a gene on a sex chromosome.

So to sum up the definition:

  Sex linkage is the location of a gene on the differential region of a sex chromosome. (this is applicable to human beings because we have PARs)

For animals in general having sex chromosomes the definition from Genetic analysis is alright.

Note: Sex chromosomes are chromosomes that have genes that have roles in determining the sex of an individual of a species.


What would cause a single white eyelash? I couldn't find a paper who could give me the explanation. Unfortunately, according to my search, it seems there are not many reported case, particularly for the younger population (<30). Would stress cause this?

What Causes Hair to Have Colour and How is Colour Lost?

The colour of hair is due to the presence of melanin, which may be found as eumelanin or pheomelanin. Melanin is produced by melanocytes and is transported to keratinocytes. The hair then grows out from a root at the bottom of the hair follicle. A hair without melanin is a grey hair. The exact specifics of how hairs go grey is quite complex and poorly understood.
The growth and pigmentation of hair grows are both regulated by many factors, including genes such as MC1R and DLX3. This provides some explanation why people of particular ethnicities or families can go grey at different times - their genetic makeup changes how quickly they go grey.
Another factor affecting hair pigmentation is reactive oxygen species (ROS). The generation of ROS (oxidative stress) has been shown to have a role in the greying of hair.. Moreover, ROS are generated by smoking, which could lead to premature greying.
Other factors that have been found to be associated with premature hair greying include UV light, vitamin B12, iron, copper, ferritin, calcium and vitamin D3 (source).

What Would Make an Individual Eyelash go Grey?

As far as I know, the regulation of eyelash growth and pigmentation is very similar to that of hair on the scalp.
Given that the regulation of hair pigmentation is controlled by genetic factors, it could be that there is a change in the function of the genes at that particular hair follicle. This could possibly involve mutations which change signaling pathways, melanin generation, etc. such that melanin is no longer transported into the hair.
There could also be an extrinsic (outside of the body) factor which has locally stopped melanin production. Perhaps at some point, there was an elevated level of ROS or UV light at that particular hair follicle. This could have introduced mutations in the genes, or could have changed how the hair was pigmented.
Alternatively, there could be death of melanocytes in that specific area, which could stop the generation of melanin. There could also be a local change in the levels of the factors associated with greying (e.g. a local vitamin B12 deficiency).

Does Stress Cause Premature Greying?

Surprisingly, despite common knowledge telling us that hair makes us go grey, there is conflicting evidence about this. Stress has been shown to make us go bald earlier but whether it also makes us go grey is not conclusively known. But given that stress has a clear negative impact on health, it's probably best not to be too stressed regardless.


Effect of steroid hormone on specific cells? As steroid hormones can pass through the plasma membrane by simple diffusion because they are lipid derived hormones, it means that they are capable of passing through every cell of our body, BUT why are only specific cells responsive against steroid hormones?

For example, all of our body cells almost contains the genes for the development of secondary sexual characters but why do only specific cells show a response against these steroid hormones because the development of secondary sexual characters occur only in specific region of our body, that is, beard formation occur only in a specific region of the face, etc.

IN SUMMARY: When steroid hormones can pass through every cell of our body then why do they show only a localized response?

The quick answer is that only certain cell types express the required steroid hormone receptors that are necessary to induce signaling and gene regulation when bound to their target steroid hormones, like estrogen, testosterone, cortisol, etc. If no receptor is present, the steroid doesn't effect any change.

The second part of the answer involves the particular signaling pathways induced by the ligation of certain receptors by certain classes of hormones. Testosterone, for example, has numerous effects across the body, from promoting the growth of hair to building muscle mass to effects on mental well-being. Testosterone and its primary metabolite 5α-dihydrotestosterone bind primarily to the cytoplasmic androgen receptor, which then translocates to the nucleus, binds DNA at hormone response elements, and alters the transcriptional activity of genes (either increasing or decreasing, depending on the gene and the cell type). Testosterone can also be metabolized to estradiol and bind estrogen receptors, which function similarly to the androgen receptor (although it can have DNA-independent effects as well).

So, depending on the cell type, receptor expression levels, other DNA regulatory elements, the presence or absence of various testosterone-metabolizing enzymes, and other factors like age, gender, etc., a single steroid hormone can have a multitude of effects throughout the body.


What is the word for a group of genes inherited together? I know the words haplotype and haplogroup, as well as genetic linkage, but...
I recently came across a new phrase describing genes which tend to be inherited as a group, and wrote it down, but now cannot find it...
Also, is there a word or phrase for genes which are expressed together?

I believe you are referring to operon?

In genetics, an operon is a functioning unit of DNA containing a cluster of genes under the control of a single promoter. The genes are transcribed together into an mRNA strand and either translated together in the cytoplasm, or undergo splicing to create monocistronic mRNAs that are translated separately, i.e. several strands of mRNA that each encode a single gene product.

There is also a term called supergene which is in a way a less strict grouping, suggesting close genetic linkage and possible functional relationship.


Do all humans have an identical nucleotide sequence for certain proteins, e.g haemoglobin? All humans have the same sort of proteins in our bodies. Take haemoglobin for example.

Is the gene coding for haemoglobin in my body identical to everyone else's gene or is there slight variations in the nucleotide sequence?

Are there examples of proteins that are always completely conserved at the population level?

It is highly unlikely that there exist any protein that is made from completely identical nucleotide sequences across the entire human population. There will certainly be regions within a gene that are highly conserved, but there is little evolutionary pressure to conserve an entire gene's nucleotide sequence across the population.

This is in part due to the fact that different codons can translate into the same amino acid. So, even if a protein is (phenotypically) identical across the human population, the genes making that protein can use different sequences to code for the same amino acids. This alone can allow for an incredibly large number of possible gene variations that can code for an identical protein.

Related resources: Neutral mutation (wikipedia) and the neutral theory of molecular evolution (wikipedia)


Relationship between lifespan and reproductive age? I remember reading a while ago that there is a "general rule" in biology between an animals lifespan and when they reach reproductive age.

In other words, an organism that reaches sexual maturity after a short amount of time (for example, less than a year) will have a short lifespan (for example, 2-3 years) and an animal that reaches sexual maturity after a long time (elephant, 10-12 years) will have a much longer lifespan (40-60 years in case of elephant).

Is there a special name for this "law" or "rule"? Are there any major papers/theories supporting it that also attempt to propose why (perhaps from an evolutionary perspective) this trend exists?

Some quick supplemental questions:

1.) Is there also a trend between lifespan and animal size?

2.) Is there also a trend between lifespan and base metabolic rate?

3.) Do the two aforementioned "trends" or "rules" have technical names that I could look up as well?

The sort of thing you're talking about would be called a Life History Invariant: a dimensionless ratio between two life history traits $A$ and $B$, such that although the traits themselves vary widely between species, the ratio $\frac{A}{B}$ is relatively constant.

Eric Charnov has written a lot about this, including a book.

One of the invariants which has been suggested is the ratio of age of maturity $\alpha$ to adult lifespan $E$. Charnov claims that it is relatively invariant within taxa, but has a different value for eg. fish vs. mammals vs. birds vs. reptiles.

From Charnov and Berrigan, "Dimensionless Numbers and Life History Evolution: Age of Maturity Versus the Adult Lifespan", Evolutionary Ecology (1990).

(If the ratio $\frac{A}{B}$ is invariant, then plotting $A$ vs. $B$ for different species on a regular graph will give you a straight line passing through the origin. The slope of the line gives you the value of the invariant.

Sometimes, in looking for an invariant researchers will instead graph the quantities on a log-log plot: they then look for whether the curve is a straight line with slope 1 (whose height gives the value of the invariant), with a good fit. This method has been criticized: the fact that some quantities are just about necessarily a fraction of other quantities (eg. you can't really lay an egg bigger than yourself), together with the fact that log-log plots "squish down" variance about the regression, opens the possibility of observing artifactual yesses. I tried to give an intuitive explanation of this criticism in a quora answer. Charnov and company have dismissed it as not applying to the invariants they found, however.)

This invariant is slightly different than the one you describe, in that they deliberately ignore pre-maturity deaths. (If infant mortality were high enough then it would be possible for average lifespan to be less than the age of maturity.) Also, they measure the ratio of pre-maturity lifespan to post-maturity lifespan $(\frac{\alpha}{E})$ instead of the the ratio of pre-maturity lifespan to total lifespan $(\frac{\alpha}{\alpha+E})$. These are just two different ways of talking about the same thing, but the former has an upper bound of 1, while the latter has no upper bound.

Finally, it's important to note that even if a quantity is relatively invariant, it can't be expected to be perfect; you have to decide how much noise you want to allow while still finding an approximate invariant interesting.


How do we know the brain flips images projected on the retina back around? Why do we turn images upside down again rather than dealing with them directly, still vertically rotated after passing through our lens?

I don't see how that would cause any problems, and how we'd ever be able to figure out if we are presented with flipped images after getting used to interacting based on visual input, whether flipped or not.

What am I missing?

The basis of this question is a common misconception, and unfortunately the accepted answer by @CHM is also based on this common misconception. The misconception is based on the homunculus falacy: the tendency for people to think that the image that lands on the retina is somehow 'assembled' and presented for something (the 'consciousness') to view. This is not the case.

As the comment by @mgkrebbs explains, there is no orientation (up or down) in the brain, there is only neural firing. The information of the visual scene is distributed over the brain, and information does not have physical properties like orientation. Although as @nico pointed out the neurons that process the information do have a spatial structure that mimics that of the retina, this is a topological property (i.e. stimuli that are close on the retina are processes by neurons that are close in V1) and such a topological property does not induce an orientation.

The root of the problem is really that the question "How do we know the brain flips images projected on the retina back around?" is a pseudo-question. Although it is grammatically well-formed, it makes no semantic sense. When the image is 'in the' (i.e. being processed by the) brain it no longer has physical properties like orientation. Thus you cannot ask if it has been flipped or not.


Is there any disease in common between human and insects? I am not asking about disease transferred by insects.

I am wondering is there any disease that commonly make both human and insects sick?

It is always difficult to prove that something does not happen, so I will restrict myself to saying that I know of no examples and think it unlikely that there will be a common viral or bacterial disease of human and insects.

Viruses are not limited to a single host, but the typical host range of mammalian viruses would not appear to extend to insects, as far as one can tell from the literature — see e.g. the Wikipedia entry on Virus.

  Viruses are by far the most abundant biological entities on Earth and they outnumber all the others put together.[134] They infect all types of cellular life including animals, plants, bacteria and fungi.[3] Different types of viruses can infect only a limited range of hosts and many are species-specific. Some, such as smallpox virus for example, can infect only one species—in this case humans,[135] and are said to have a narrow host range. Other viruses, such as rabies virus, can infect different species of mammals and are said to have a broad range.[136] The viruses that infect plants are harmless to animals, and most viruses that infect other animals are harmless to humans.[137]

Likewise for the host range of bacterial pathogens, judging from articles such as an article by Baümler and Fang in the Cold Spring Harbor Perspective on Medicine.

One general molecular reason for expecting a limited host range that would exclude insect/human pathogens relates to the means by which the pathogens enter the host cells. Quoting, for example, from the abstract of an article by JM Casasnova:

  To initiate the infective cycle, the viral genome must therefore translocate from the viral particle to the cytoplasm. Via distinct proteins or motifs in their outermost shell, the particles attach initially to specific molecules on the host cell surface. These virus receptors thus mediate penetration of the viral genome inside the cell, where the intracellular infective cycle starts. The presence of these receptors on the cell surface is a principal determinant of virus host tropism.

The membrane proteins that act as receptors generally differ between related members of a species, but mutations can allow the viruses to cross species barriers. However the extreme difference in cellular structure and biochemistry between insects and humans make it unlikely that this could happen, even if the cell type and protein still exist in common. Consider, for example viruses such as Hepatitis A, B and C which infect the human liver. My own favourite insect — Drosophila melanogaster — does not have a liver as such, its functions being served by the insect fat body.

I am less familiar with other aspects of the viral life cycle that relate to physiology (my background is chemical) but these clearly differ and would affect modes of transmission, for example respiratory and sexual.

These latter considerations will also apply to pathogenic bacteria. As an anecdotal conclusion to an imperfect answer, I would mention the bacterial diseases of silkworms that affected the French silk industry in the 18th century. There are several accounts of Louis Pasteur being called in to eradicate the disease but these contain no suggestion that the workers breeding the worms contacted the disease.

Tribute to Pasteur for ‘saving’ the silk industry at Ales, nr. Nîmes, France


How long does it take for DNA to degrade Can i still use 3-4 years old bacterial DNA template for my PCR? They were kept in -20 all this while. Will the DNA degrade?

Degradation of DNA is gradual, but continuous, even in the freezer. However, they can sequence DNA from ancient animals in permafrost, or Neanderthal teeth. Fresh is always best, but there is no reason not to try PCR on your samples.


What is the standing genetic variation? I am reading this review. In the first part, the author introduces Standing Genetic Variation, described as:

  STANDING GENETIC VARIATION Allelic variation that is currently
  segregating within a population; as opposed to alleles that appear by
  new mutation events

Does it mean that in adaptation the allelic variation is already present (not created by mutations) and in adaptation it prevails over the others?

Thanks

Standing genetic variation is when there is more than one allele at locus in the population at the time-point in question. When an allele goes to fixation there is no standing genetic variation at the locus until new mutations occur. Loci where alleles are not fixed are described as having standing genetic variation.

  "Standing genetic variation: the presence of more than one allele at a locus in a
  population."

from Barrett and Schluter 2007


Why are sperm cells not attacked by the female immune system? Whenever a foreign particle enters into someone's body, it is attacked by the white blood cells. I just want how it is that, when sperms enter the female body, they are not attacked by the the woman's immune system?

Studies show semen does mount a considerable immune response in the female mucosa, however:

  Seminal plasma redirects the differentiation of human dendritic cells (DCs) toward a regulatory profile. By promoting a tolerogenic profile in DCs, seminal plasma might favor fertility, but might also compromise the capacity of the receptive partner to mount an effective immune response against sexually transmitted pathogens.

Semen promotes the differentiation of tolerogenic dendritic cells.


Kidney failure → Inhibition of Na+/K+ pump → Heart failure I read in my biology book:

  Due to kidney failure, the concentration of K+ in the body increases. This can lead to heart failure too.

But there wasn't any explanation to the mechanism of this phenomenon. So, I took help of the internet, found out about the Na+/K+ pump and its role in muscle contraction on the Wikipedia page.

But, there wasn't any direct mention of the relation between inhibition of Na+/K+ ion pump and kidney failure. After some brainstorming, I hypothesized the following mechanism:

Due to kidney failure, the aldosterone-catalysed mechanism for keeping the Na+ concentration static in bloodstream stops. So, Na+ ions filtrated by the nephron can't go back to the bloodstream, resulting in a decreased concentration of Na+. Then, the decreased potential difference between intra and extracellular space, in terms of Na+ ions, inhibits the Na+/K+ pump. As muscle contraction is dependent on the Na+/K+ pump, heart muscles stop to work.

Is my hypothesis right?

Hyperkalemia (too much blood K+) caused by kidney failure is because the kidney is not clearing excess K+, and most K+ excretion is by the kidneys. Usually kidney failure alone isn't sufficient to cause hyperkalemia (Lehnhardt and Kemper,
 2011), and note that kidney failure can cause problems via many other mechanisms besides hyperkalemia.

The reason that hyperkalemia causes problems with heart and other muscle function isn't directly because of the Na+/K+ pump, but because of how the electrical potential of cells controls contraction. Cardiac myocytes, like most cells, have a negative resting potential, with high K+ inside and low Na+ and Ca2+ inside, and a resting conductance that is higher for K+ than the other ions. When the cell is depolarized to around -40mV, a rush of Na+ and Ca2+ comes in that further depolarizes the cell and also causes the muscle contraction.

Normally, this "action potential" is terminated by opening K+-channels, which returns the cell to a hyperpolarized/resting state by letting K+ ions flow out, ready to fire another action potential and contract again. However, the resting potential is determined by the Goldman equation and depends on the concentration of each ion both inside and outside the cell. The reversal potential for K+ depends on there being a lot of K+ inside the cell, and very little K+ outside the cell. Therefore, it takes a large negative potential to keep K+ in equilibrium. As the K+ concentration outside the cells increases, the equilibrium potential for K+ gets closer to 0 mV. Eventually, cells can't repolarize after contraction and effectively stay in "contraction mode" without relaxing.

Although the Na+/K+ pump is somewhat dependent on the concentrations of Na+/K+, the typical role for that pump is to push K+ ions into cells and pull Na+ ions out. If blood K+ is high, that will not do anything to prevent the Na+/K+ pump from operating, so suppression of that pump is not having any mediating role in this process.

As a side note, KCl is used in lethal injection in the United States as the final drug administered, which stops the heart by causing immediate hyperkalemia.


What is the best argument for maximum parsimony method in phylogenetic tree construction? Beside the fact that maximum parsimony is computationally cheap, what other good arguments are there for it? Is there any model behind this principle? Why would one expect this principle to provide right phylogeny in any situation at all ?

The idea of parsimony is that when constructing phylogenetic trees a simple hypothesis (e.g., four evolutionary changes are necessary to connect two taxa) is more likely to be true than a more complex hypothesis (e.g., 15 evolutionary changes) (source: Berkeley University).

The reason is that for a certain taxon to evolve, there must be a certain number of evolutionary changes. In the end, this happens by more or less stochastic processes (Dingli & Pacheco, 2011) that randomly generate genetic changes (mutations). The characteristics of better fit individuals survive, while those of the least fit are terminated from the gene pool. Hence, every additional change that must be adopted to create a new taxon from another means that the chance that that happens decreases exponentially; it's all a matter of statistics. The less the number of changes needed, the higher the chance that that might have actually happened.

Reference
- Dingli & Pacheco, BMC Biology (2011);9:41


Does photosynthesis begin instantly when a plant is exposed to light? I'm curious to know if the process of photosynthesis has a "ramp-up" time to become useful to a plant, or if it begins instantaneously when the plant is exposed to light after a period of darkness.

For example, if I'm growing a plant indoors using artificial light, does the plant start converting CO2 the very moment I switch on the light, or does it take a certain period of time for the reaction to reach a critical momentum for the plant to be able to produce sugars?

Or, as a thought experiment, if I turned on the light for 10 minutes, would the plant produce roughly the same amount of sugars as if I toggled the light on for 1 minute, then off for 10 minutes, 10 times in a row?

This is a really interesting question! It gets to the heart of how photosynthesis works.

First, note that whether or not the plant will immediately start producing glucose depends on a variety of factors (what type of plant, what type of light). For example, many succulents undergo CAM photosynthesis (Crassulacean Acid Metabolism) in which light capture and CO2 fixation are temporally separated (the former during daylight hours and the latter at night). Additionally, artificial light comes with different wavelength compositions (ratio of red to far-red light  can differ) and photosynthesis rates will change accordingly read more here.

But I haven't yet addressed the heart of your question: how long does it take for a plant to start photosynthesizing once it is exposed to light? To think about this, consider what is actually happening when light hits a leaf. Light energy is absorbed by pigments in the chloroplasts, which transfer energy to neighboring pigments until an electron is transferred to a reaction center. From here, "light reactions" of photosynthesis continue and usable chemical energy is obtained. From there, the CBB cycle (sometimes called the Calvin Cycle, Calvin-Benson, or "dark" reaction) continues, which is where the CO2 from your question comes into play, and 6-carbon sugars are produced. It isn't a matter of "ramping up", so much as completing this series of chemical reactions.

So now, it is time to consider your thought experiment. Let's say that you have a bean plant in your kitchen (C3 photosynthesizer), and you conduct your experiment shining a white-light lamp on the plant with the experimental conditions as described. I believe that you would produce roughly the same amount of sugars in each because glucose synthesis occurs on the order of seconds (~30s). If you exposed your bean plant to white light for only 5-second increments, there would not be time to produce the energy needed to complete the CBB cycle.

Aside: the experiments that first elucidated the CBB cycle were conducted by exposing cyanobacteria (a photosynthetic bacteria) to labeled (heavy) carbon, and exposing it to light for a few seconds, and characterizing which compounds were produced from that heavy carbon within that few-second time frame. Read more about that experiment in the previous link. It sounds like Calvin himself wondered the same thing you did!

For further reading on the basics of plant physiology, including photosynthesis, I always recommend the plant bio "bible": Plant Physiology and Development by Taiz L., Zeiger E., 2010. I still consult it often.

Hope this helps. Stay inquisitive!


Is there a term for the entire system of moving oxygen around? The respiratory system brings oxygen to the blood, and also can include stuff like nicotine from smoking.
The circulatory system brings oxygenated blood (and all its little friends) to wherever they're needed.

Both the respiratory system and circulatory system are extremely important in keeping hypoxia from happening, but I'd like to focus specifically on the system of oxygenation.  I don't want to include the systems of smoking, or moving around nutrients.
Is there are term for the "oxygenation" "stop hypoxia from happening" system?  Basically just the parts of the respiratory and circulatory systems that move oxygen?

Short answer
"Oxygen homeostasis" is the best I can think of.
Longer answer
Don't forget the other half of the oxygen equation: carbon dioxide is an important waste gas and failing to remove carbon dioxide is just as much a problem as failing to deliver enough oxygen.
You could refer to "oxygen homeostasis" if you wanted to just refer to keeping enough oxygen in distal tissues; as you describe, both respiratory and circulatory systems are relevant for oxygen homeostasis. However, it's hard to separate from the rest of the gas exchange system. Carbon dioxide is very important in determining the rate of respiration, for example, as well as the release of oxygen in peripheral capillaries. Therefore, even if you want to focus on just oxygen, carbon dioxide is going to come up no matter what! As is the function of the vasculature, heart, and lungs: even if these organs have roles outside of delivering oxygen, their functions apply to all gasses exchanged and everything that is transported in the circulatory system. Very little happens in these systems that will only affect oxygen delivery without affecting anything else.
The efficiency of oxygen delivery also depends on what exactly you're inhaling; I find it a bit bizarre to include "smoking" as seemingly part of ordinary biological function, but if you want to go there it's reasonable to consider the role of carbon monoxide and anything else that may interfere with oxygen binding to hemoglobin.


Could silicon oil block Na+ ion channels in the membrane of an axon and prevent Na+ influx? Could silicon oil block Na+ ion channels in the membrane of an axon and prevent Na+ influx?

I have been wondering if Na+ influx could have been a diluting factor in anterograde fills.  If so, could coating the axon with silicon oil prevent this?

No, silicon oil couldn't block an ion channel. Oil is a nonpolar substance, just like the membrane lipids, so if you can get your oil to that cell, it will mix with the lipids within the membrane. The ion channel, which sits in the membrane, too, is rather closed to the membrane interior and opens to the inside and outside of the cell which, contrarily, is a polar solution of soluble molecules in water. So, to block one of the openings you better have a polar molecule that is water-soluble.

http://en.wikipedia.org/wiki/Ion_channel

http://en.wikipedia.org/wiki/Polarity_%28chemistry%29


Why was the evolution of large, slowly reproducing organisms preferred? One of the very basic facts that Darwin pointed out was about the life span of organisms. Organisms with smaller lifespan reproduce quickly and hence variations are produced faster. This helps in faster evolution.

One of the main goals of living organisms is to reproduce, this fact being the backbone of neo-Darwinism.
For organisms with longer life span, say humans, the amount of time required for new generations to come up, as well as the energy requirement is high, much higher if compared to bacteria. Then why did evolution of complexity arise if bacterial life forms could survive in harsh conditions and reproduce and mutate faster?

The simple answer is that the evolution of large, slowly reproducing organisms is not preferred: it is simply not selected against.

The key mistake in your thinking is this statement:

  One of the main goals of living organisms is to reproduce

Most living organisms have no such goal, they simply take actions that have, historically, led to the continuation of their lineage.

In a complex world, there are many different strategies that can lead to survival and propagation of an organism, and cooperation between cells is one of them.  Even simple bacteria often form large multicellular aggregates, which can provide physical advantages for their members over dissociated individuals, such as resistance to physical damage and formation of protected microclimates. The inside of your body is another such protected microclimate. So multicellularity can be quite advantageous.

As for limiting reproduction: remember that the closest competitors every new organism has are its own relatives, who occupy the same space and compete for the same resources.  Even bacteria will often limit their reproduction when resources are limited. Reproduction also takes significant resources. A faster reproduction then, is also not necessarily advantageous for long-term survival.

Bottom line: neither large nor small, fast nor slow is preferred.  Instead, the study of evolution predicts that we will see what we do see: a multiplicity of forms and strategies adapted for different niches in the ecosystem formed by their interactions with other species and the external environment.


Electroporation of one-cell embryo? Would electroporation be successful on a one/two-celled mouse embryo? If it would, what buffer could be used and what percentage of cells would be viable?

Thank you.

The buffers are usually supplied with the electroporation instrument; at least Lonza provides buffers for different types of cells. Single cell electroporation techniques exist, but they have been mostly done on neurons.[1,2]

You can also try microinjection but it requires some practice. This study reports a transfection agent called VisuFect which can be used for zygotes as well.

I am not very sure about the success rate (AFAIK it is not that good) but I think it is anyway risky with organisms which do not produce a lot of embryos.


To what extent can bacteria actually see? I found some popular articles (e.g. nbcnews and iflscience) that bacteria can "see," but I highly doubt it's in the same way as people do just from looking at the limitations in the vision of small animals like insects. So what exactly are bacteria capable of "seeing" or what are the limitations of their vision?

Simple answer is that many simple organisms, including bacteria, carry light-sensitive molecules. One example is halorhodopsin (not bacterial but archaeic). This is a molecule, light-gated ion pump, that reacts to light, thus allowing organism to react to photons by changing concentration of certain ions inside the cell.

Study from Stanford described similar molecule found in bacteria.

In conclusion, if by "vision" you understand ability to react to light in the visible part of the spectrum, then a lot of organisms possess such ability. However, they lack other crutial parts of human vision.


Why do obese people tire quickly? Fat people have a large amount of calories (energy) stored, but I have noticed all time when they do physical activities they get tired fast in comparison to fit people - why does this happen?

Fatigue on exercise is proportional to unmet demand for oxygen and glucose (sugar/fuel).

In people who are "fat":

They typically do less exercise. Therefore their cardiovascular system is not conditioned with the heart being able to cope with increased exercise i.e. it is unable to beat more efficiently and instead must beat A LOT more faster to cope consuming more oxygen and glucose. Even at rest, they will typically have a higher resting rate. They also have less efficient muscles (i.e. the muscles themselves can't breakdown energy as well, use it as well and the body isn't as great at picking the right set of muscles)
The fat itself can compress vessels carrying blood. This pressure increases blood pressure. This is worsened by a typical high diet of salt and again by typical lack of exercise. Higher blood pressure means the heart has to beat harder and faster to pump blood around the body
They weigh more so each movement requires A LOT more energy. Their resting metabolic rate is higher than a thinner person as is any exercise they do.
On exercise they do not lose heat fast enough. This impairs the breakdown of glucose and also more energy is required to lose the excess heat
They may be subclinically diabetic. Their body may have lots of glucose floating around in the blood but they can't use it because their muscles can't absorb it.
They have far increased rates of build up of fatty plaques on the blood vessel walls. This narrows the vessels and only multiplies with all the other problems
Then there's lots of other more minor but very important reasons like psychological (reduced capacity to brave through fatigue), reduced sleep meaning a higher baseline of tiredness (in the extreme side caused by obstructive sleep apnoea), increased rates of smoking (which does millions of things to reduce exercise capacity)


Cancer cure statistics questions I have a question about cancer cure statistics. Many of the cancer literature or databases I have come across speak about 5 year or 10 year survival rates. In this case survival means that the patient with cancer is still alive 5 or 10 years after diagnosis. I am in need of references about the statistics which explain what is the percentage of people in these groups who are in progression-free survival group and disease-free survival group. That is for instance among the cancer patients which survive for some X years, who are completely cured of cancer (which means that the cancer is completely cured and has not reoccured with in this X years).

Update: USA data is preferred

Thanks

I would caution you against using phrases such as "completely cured" or even "cured". This goes beyond our technical ability to detect the presence of tumor cells within someone's body. All we can conclude is progression-free survival (i.e. living with cancer that does not get worse) or disease-free survival (i.e.  or no signs or symptoms of the tumor). Many of these data are included in cancer trials along with overall survival rates. Some general statistics for many groups of cancers can be found here: http://www.cancer.gov/statistics/find

And a glossary of terms used in reporting cancer statistics here: http://www.cancer.gov/statistics/glossary


Are there known life forms that are able to transform mechanical energy into chemical energy? Are there known life forms that are able to transform mechanical energy into chemical energy?

This question asks a similar subject, but more specific and has no answers.

The background of this question are thoughts about hypothetical life on tidally locked exoplanets of red dwarf stars, where light for photosynthesis is scarce but mechanical energy (storms and/or water currents) aplenty.

There are no known life forms that use mechanical energy as a primary form of metabolic energy (i.e., for generic cellular functions). Many life forms are sensitive to mechanical disruption in some way, so they do utilize mechanical energy, but in a very limited fashion (@David's answer touches on this), and of course many organisms have life cycles that somehow depend on mechanical transportation (seed/spore dispersal, traveling on the wind or ocean currents, etc).

I think the main physical problem is that mechanical energy just isn't available to biological cells in a form that can be converted to substantial chemical energy. They are small, and tend to have other great benefits for being small.

To use an ocean wave as an example, there is very little or no perceptible movement for a cell in that wave, besides an apparent increase and decrease in the force of gravity. The top and bottom of the cell are moving together with the flow of water, so there is no differential to operate on.

An E. coli weighs about 1 picogram. If it could capture all of the energy from falling from 1km in the air on earth, assuming no uncaptured aerodynamic drag, that would be about 10-11 joules.

If there are ~3000 kJ/mol of energy available from burning glucose, that means about 5 × 10-21 joules per molecule of glucose, so about 20 billion glucose molecules, which sounds like a lot but it is only 1 femtogram, 0.1% the weight of the cell.

Also note: in @David's answer he makes a very good point that in a way, using mechanical force to open a channel is indeed a form of energy usage and therefore a proof of concept that this could happen. To put that process in the same ballpark, this source (originally mentioned by @GerardoFurtado) gives the work necessary to open one of these channels at around 8 × 10-22 joules. The open latency for those channels is under 50 microseconds, but that still greatly limits the number of possible cycles per unit time. Chemical energy is just substantially more dense than mechanical energy is: that's why gunpowder superceded catapults (and even the trebuchet..).


What causes spontaneous muscle twitches? Sometimes a small region of my body starts shaking, without any reason and then stops abruptly. Apparently this is a common phenomenon (source: NIH).  I researched its cause for a bit and came to know that it is because of nerve excitation.

Why do those nerves get spontaneously excited in the first place, without any conscious, voluntary, internal stimulus being presented?

Short answer
Spontaneous muscle twitches are thought to be caused by spontaneous activation of motoneurons controlling the muscles.

Background
Spontaneous muscle activity (twitching) is referred to as muscle fasciculations. Most commonly, they are benign, but they can be associated with certain pathologies too, such as ALS.

Fasciculations are thought to originate due to spontaneous activation of muscle fibers due to processes in the motoneurons. At the axonal endings there are synapses that junction onto the muscle. The axonal tips of motoneurons are thought to be highly sensitive to depolarization (electrical firing), which is what triggers acetylcholine release and muscle contraction.  The complicated process itself takes a small fraction of a second.  If any of this happens involuntarily, then the muscle fiber contracts spontaneously (source: ALS Association).

Specifically, it is thought that spontaneous depolarization of motoneurons are the cause of fasciculations. This decreased firing threshold can be the cause of disease, disrupted ion homeostasis in the body, fatigue, drugs and other causes (Blum & Rutkove, 2007).

Note that spontaneous / random activity in neurons is not only possible, it is quite common. Especially in neurons close to firing threshold, such as the motoneurons responsible for muscle activity, slight perturbations in ion concentrations inside or outside the cell can trigger an action potential. Further, channel opening is a stochastic process, meaning that even voltage-gated Na+ channels can open without a depolarization being present; although the chance is slim that will happen, it can statistically still happen. Stochastic processes like this can cause neurons to fire spontaneously, without a stimulus being present.

Reference
- Blum & Rutkove, The Clinical Neurophysiology Primer, Springer (2007)


How much energy is required to blind someone? As I understand the ravages of sunlight upon the (human) eye; the cause of ocular damage and blindness is too much energy delivered to the cones and rods that ultimately make up our eyes; so the questions arise:

How much light can a (human) rod take?

How much light can a (human) cone take?

Light can affect retina in many ways [1]:

photothermal mechanisms - exposure to intense flashes of less than 20 microseconds that cause a rise in temperature of at least 10 degrees Celsius [5];
photomechanical mechanisms - exposure to flashes shorter than 5 nanoseconds [5];
photochemical mechanisms - light is absorbed by a chromophore and leads to the formation of an electronically excited state of it, resulting in chemical transformations [5].

The retina is more susceptible to light induced degeneration at lower wavelengths [2, 8]. The damage degree also depends on intensity and exposure duration. 12 hours a day of more than 500 lux light, more than three consecutive days can affect rat retina [3]. 2 hours  exposure to white light of 3000 lux has lead to apoptosis in rats retina [4].

Sunlight irradiance is about 11 W/cm2 (ranges between 1.5 and 122 W/cm2) and causes damage when exposure time is tens of minutes or even less [5].

Light induces apoptosis by different mechanisms:

  Intense light triggers cell death in cones and rods by two distinct mechanisms: rapid, necrosis-like cell death occurs in cones; prolonged, apoptotic death is displayed by rods. However, the areas of cone and rod loss coincide, suggesting some interrelationship [6].

Cones and rods have different vulnerability [7].

References:

Youssef PN, Sheibani N, Albert DM. Retinal light toxicity. Eye (Lond). 2011 Jan;25(1):1-14. doi: 10.1038/eye.2010.149. PubMed PMID: 21178995.
Rozanowska, M. B. (2012), Light-Induced Damage to the Retina: Current Understanding of the Mechanisms and Unresolved Questions: A Symposium-in-Print. Photochemistry and Photobiology, 88: 1303–1308. doi: 10.1111/j.1751-1097.2012.01240.x
Jin X, Wu L, Zheng H, Mishima S. [Retinal light damage: I. The influences of light intensity and exposure duration at moderate and low intensities of cyclic light]. Yan Ke Xue Bao. 1998 Dec;14(4):215-9. PubMed PMID: 12579740.
Remé CE, Weller M, Szczyesny P, Munz K, Hafezi F, et al. Light-induced apoptosis in the rat retina in-vivo. In: Anderson RE, LaVail MM, Hollyfield JG, editors. Degenerative Diseases of the Retina. Plenum Press; New York: 1995. Via http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831109/
Malgorzata Rozanowska, Bartosz Rozanowski, Michael Boulton. LIGHT-INDUCED DAMAGE to the RETINA (2009). Available from http://www.photobiology.info/Rozanowska.html (accessed 20.07.2014).
Cortina MS, Gordon WC, Lukiw WJ, Bazan NG. Light-induced photoreceptor damage triggers DNA repair: differential fate of rods and cones. Adv. Exp. Med. Biol. 2004;533:229-40. PubMed PMID: 15180269.
Okano K, Maeda A, Chen Y, Chauhan V, Tang J, Palczewska G, Sakai T, Tsuneoka H, Palczewski K, Maeda T. Retinal cone and rod photoreceptor cells exhibit differential susceptibility to light-induced damage. J. Neurochem. 2012 Apr;121(1):146-56. doi: 10.1111/j.1471-4159.2012.07647.x. PubMed PMID: 22220722.
Kuse Y, Ogawa K, Tsuruma K, Shimazawa M, Hara H. Damage of photoreceptor-derived cells in culture induced by light emitting diode-derived blue light. Sci Rep. 2014 Jun 9;4:5223. doi: 10.1038/srep05223. PubMed PMID: 24909301.


Is there any small animal that can jump over a meter high/long? By small, let's say less than 5 cm body length. I always thought that grasshoppers were the highest absolute jumpers in this class but the highest jump according to this article is 0.7 m...

no animal smaller than 5 cm can jump higher than 1 meter. grasshoppers and locusts have wings which supposedly disqualifies them. https://www.guinnessworldrecords.com/world-records/highest-jump-by-an-insect.
The immense mechanical power that would be required for any animal to jump so high with such a small size is unbelievably high which is why they have developed different evolutionary adaptations. not to mention that the terminal velocity of such a small creature is very low so a jump would quickly become a fall due to the air molecules slowing them down. https://www.youtube.com/watch?v=f7KSfjv4Oq0


Where do most mutations come from, mitosis or meiosis? According to this (old) paper there are 10 times more mutations during meiosis than during mitosis. One reason for that is that recombination often causes replication error and therefore mutations. However, in many multicellular organisms, germ cells undergo many cell divisions (mitosis during development) before finally undergoing meiosis.

I think that intuitively many people (me at least) think of new mutations* that are transmitted to the offspring as mutations occurring during meiosis. I would like to have a notion of how important are the two processes (mitosis and meiosis) in generating heritable new germ-line mutations in multicellular animals.

Let's consider humans for example. Out of 100 new germ-line mutations transmitted to the babies, how many of those mutations occurred during mitosis (during the development)?

*I call "new mutations", any mutation that is transmitted to a baby but that was not present in any of the two eggs of the parents (even before the parents started the gastrulation).

@Remi.b I think we can do better than 1962. Let's fast-forward here to 2014, in the post-genomic era.  I think this paper provides some data relevant to your query: Possible mechanisms for Chromothripsis .


Can there be an equilibrium between humanity's increase of carbon dioxide output with plants since plants harness CO2? Is it possible that, prior to hitting a thermal equilibrium in the atmosphere, the increase in CO2 that humanity puts out every year will come to an equilibrium due to the consumption by the world's plants, which may respond by growing, reproducing and feeding more off of the additional CO2 in the atmosphere at a faster rate?

Yes, with 2 caveats.

More CO2 encourages plant growth up to the local plants' limit. After that limit, the plants are saturated and extra CO2 backlogs into the air. If you intend to prevent atmospheric CO2 buildup, you're better off gradually supplying CO2 rather than deploying it in large surges.

The other caveat is dead trees and other plants that should be harvested or logged to make way for new growth (while providing lumber, fuel, and employment).


If nerve consists of many axons, where are then their soma located? This question has haunted me for two years.

Wikipedia mentions :

  A nerve is an enclosed, cable-like bundle of axons (the long, slender projections of neurons) in the peripheral nervous system. A nerve provides a common pathway for the electrochemical nerve impulses that are transmitted along each of the axons to peripheral organs.

Okay, my book also defines like that. But if the nerve runs only with bundles of axons, where then are their soma located?

They say nerves are formed of many axons bundled together. Now, if there are axons, there must be soma, but they do not form nerve & hence are not present in nerve. So, where are they? Are they present at the beginning of the nerve?

Also, nerves communicate with each other. Books picture this as two neurons one above other; the above one sends impulse through its terminals to the dendrites of the neuron below it. So, how do these two neurons constitute a nerve?? After all, they now contain the cyton?? So, how do neurons one above other form nerve as they now contain the soma??

PLz explain.

Neurons or nerve cells typically have a dendritic region, an axon and a cell body. The axon is also referred to as a nerve fiber. The axon is typically the longest structure, while the dendrites are mostly situated close to the cell body. See the following figure 1:

Schematic of a nerve cell. Source: Prof. Brown.

Axons often bundle into nerves. For example, the peripheral nervous system contains many nerves. The cell bodies of the neurons that feed their axons into a nerve are organized into ganglions outside the nerve (Fig. 2).

The peripheral nervous system and the location of the ganglia. Source: Miami College.


What is the Importance of Acid Alcohol and Sodium Bicarbonate during staining? I've just learnt about staining during a histology class and I'm confused.
Why do we have to add acid alcohol and sodium bicarbonate to the tissue during Hematoxylin & Eosin staining? Is there any difference if we don't add them at all and just skipped to eosin instead?

This is described with better detail (and better prose) in John Baker's classic description at StainsFile, but to summarize:  The procedure you're describing is a regressive hematoxylin stain with Harris hematoxylin.  To start off with, let's bear in mind that hematoxylin, a compound from the wood of the logwood tree, is actually used as hematein, by oxidizing it with sodium iodate.  (The colorless hematoxylin would naturally "ripen", oxidize over 4-10 weeks in the presence of air, even without that step, but this is more controllable)  Additionally, aluminum ions are added as a mordant, creating hemalum by binding =O and -OH on the hematein.  The Al atom is what actually binds to something in the nucleus (I found reference to lysine side chains of histone proteins and the phosphate of the DNA - I haven't sorted this part out yet).
When acid is added, it competes with aluminum, which can be thought of as Al3+.  The real bonding may be more covalent than that, but that point is considered controversial.  For whatever reasons, the H+ interferes with the Al3+ mediated attachment of stain to tissue, especially at sites of background attachment (differentiation).  The hematoxylin washes away somewhat, leaving lighter, more specific staining.  (this tactic is called a regressive stain, and is certainly not needed to do the procedure.  This is very much more art than science at this point...)
But ... the acidic hematoxylin has a reddish color, and it isn't as blue as it can be unless it is neutralized to around pH 8 - hence the second step with bicarbonate, though often plain tap water can be used.  That is an ordinary instance of a dye changing color with pH, and can be called "bluing the hematoxylin".


Where are the statistics for vaccine side effects? My son told me that that during a discussion at school someone mentioned statistics about side effects of vaccines (I assume that the discussion was about standard vaccines in France). The numbers were completely off (1/100 "illness", 1/100 "death" - again, these numbers do not make sense).

I wanted to provide him facts to rationalize (quantify) the discussion but it is now an hour I am searching on French, Canadian and US official sites (as well as WHO) and I cannot find any statistics on side effects (from mild to mortal).

I understand that "side effects" and "vaccines" are general concepts but I want to start with anything to just show the error. Let's say that "side effect" is anything from "reasonably impacting" (so not an arm which hurts for 48 hours) to death, and "vaccines" is anything from the typical set a child will get.

Is there a place where such statistics are available?

Please note that I am not talking here about "vaccines cause autism" (there is plenty of information about that) or "vaccines are not useful" (plenty of comparative studies as well). I also understand that vaccination is a pro-vs-cons decision, I have a hard time finding the "cons" in the form of numbers.

(World Health Organisation, 2014. p. 2) shows the adverse effect (side-effect) rates for the MMR vaccine. For instance, fever  between the 7th to 12th day after vaccination occurs in 5 to 15% of vaccine recipients and rashes occur in 2-5% of vaccines, etc. Page 6 summarises the results in a table. As you point out, the adverse effects are variable in severity and dependent on the particular vaccine; an organisation like the WHO will take into account the risk and severity of these adverse effects before recommending the use of the vaccine. And as you point out, it is not believed by the scientific community at large that vaccines have links with autism.
References
World Health Organisation. (2014). Information sheet observed rate of vaccine reactions measles, mumps and rubella vaccines.


Why does Taq polymerase add 3' adenine overhangs? Is there a mechanism for the preference of Taq polymerase to add a non-templated 3' adenine (overhang) instead of other bases?

Non-templated terminal addition by certain DNA polymerases is apparently dependent on the base stacking between the incoming base and the existing duplex (Fiala et al., 2007*). This was verified by using a non-base-pairing (but better stacking) nucleotide analogue called deoxyribo pyrene nucleoside triphosphate (dPTP). Adenine seems to have a higher efficiency of base stacking compared to other three bases:  A (1.0), G (0.7), T (0.6), and C (0.5)

It was also verified that the preference for dATP did not depend much on the terminal base-pair of the duplex with the incorporation probabilities being:

79% dATP 16% dTTP, 3% dCTP, and 2% dGTP when the last base pair is A-T (A is 3'), and
81% dATP, 8% dTTP, 8% dCTP, and 2% dGTP when the last base pair is G-C

Fiala, Kevin A., et al. "Mechanism of template-independent nucleotide incorporation catalyzed by a template-dependent DNA polymerase." Journal of Molecular Biology 365.3 (2007): 590-602.

*They had used the Dpo4 polymerase from Sulfolobus solfataricus as a model because it is a known lesion bypass polymerase and its kinetics and structure are well studied.


Parasite? or a possible home infestation? I found this bug on my bed tonight.  It's smaller than a sesame seed. 6 legs and 2 antenna.

Is this causing my dog and I to itch? Should I be concerned?

It is a minute pirate bug, in the family Anthocoridae. https://en.wikipedia.org/wiki/Anthocoridae They are generally thought to be beneficial insects, in that they are predators of pests. Do you have some house plants that may be infested with something else they are feeding on (like aphids)? Unfortunately, minute pirate bugs do bite, and the bite is painful. https://hortnews.extension.iastate.edu/2017/10/minute-pirate-bugs-are-biting-argh
But these are not human parasites, and I would not be concerned. Just find what they are feeding on, and take care of that.


What is the difference between spidroin-1 and spidroin-2? So I'm doing a research project for my school and I'm trying to decide on the exact nature of the project. My current plan is to try to genetically engineer E. coli or Yeast to produce spider silk protiens. However when trying to find an appropriate gene for my project I learned that the common house spider's silk has two different spidroin protiens. Just by a simple google search I can't tell the difference. So, what is the difference between spidroin-1 and spidroin-2

I've looked into literature on this. Wow, there is a lot of research on this. Here's a quick summary:

Functionally they are very similar. Both are fibrous proteins. Together they constitute spider silk. Sp-1 and Sp-2 are two different genes, often present in multiple copies in the genome, depending on which spider species you consider. They differ in amino acid content and are post-translationally modified differently. Sp-2, for instance, is heavily modified. There also exist different transcriptional isoforms of these proteins. It seems quite complex.

There are also different types of silk. You may be referring to major ampullate silk, which is only one of six different types of silk fibres spun by the spiders of the genus Nephila. Only this one contains major ampullate spidroin-1 (MaSp1) and major ampullate spidroin-2 (MaSp2).

Excerpt from one paper on the subject, which lists some differences:

  MaSp1 and MaSp2 are large proteins of about 250 to 350 kDa that share
  a general domain architecture. Both proteins contain a large, central, repetitive domain that
  consists of approximately 100 tandem copies of a 30 to 40 amino acid
  repeat sequence. The consensus repeat sequences for both MaSp1 and
  MaSp2 are glycine-rich and end in poly-alanine motifs (usually four to
  seven residues long). For MaSp1, the consensus repeat includes (GGX)n
  motifs (where X = A, L, Q, or Y) and very low proline content. In
  contrast, the MaSp2 consensus repeat has significant proline content
  and characteristic motifs such as GPG and QQ.
  The repetitive domains of different spidroins display a relatively
  high level of amino acid sequence variation that has been implicated
  in providing the elasticity and toughness that is characteristic of
  the different fibers.

It is possible that different amounts of Sp-1 and Sp-2 are combined to tune the elasticity and toughness of the silk. I have no idea whether the mechanical properties of silk are changed by the spider to suit the context (e.g. elasticity in windy conditions, or whether the content changes seasonally in response to temperature differences). That would make for a cool research hypothesis.


Why did high A+T content create problems for the Plasmodium falciparum genome project? The main paper for the Plasmodium palciparum genome project (Gardner et al., 2002) repeatedly mentioned that the unusually high A+T content (~80%) of the genome caused problems. For example they imply that it prevented them using a clone-by-clone approach:

  Also, high-quality large insert libraries of (A + T)-rich P. falciparum DNA have never been constructed in Escherichia coli, which ruled out a clone-by-clone sequencing strategy.

And that it made gene annotation difficult:

  The origin of many candidate organelle-derived genes could not be conclusively determined, in part due to the problems inherent in analysing genes of very high (A + T) content.

Question:
What is the biological significance of high A+T content, and why would it cause problems in genome sequencing?

Ref:
Gardner, M.J., Hall, N., Fung, E., White, O., Berriman, M., Hyman, R.W., Carlton, J.M., Pain, A., Nelson, K.E., Bowman, S., Paulsen, I.T., James, K., Eisen, J.A., Rutherford, K., et al. (2002) Genome sequence of the human malaria parasite Plasmodium falciparum. Nature. 419 (6906), 498–511.

The sequencing technologies that were developed in the last 20 years have a range of optimal use at an average A+T/G+C rate. Both highly AT-rich and GC-rich regions are complicated to process by the different sequencing technologies. Each technology has different ranges of usage, but to name one, Illumina technology prefers sequences in the middle range. If you try to sequence an AT-rich genome with the Illumina standard protocol, you will sequence an incomplete genome, the fragments of which are not a perfect reflection of the original complete genome. Other technologies claim to be completely unbiased to nucleotide content. Pacific Biosciences is one of them, and people seem to agree on that claim, after having analyzed the data that is produced by their machines. Oxford Nanopore Technologies claims that they have almost no biases, but as of today (2012-06-13), there is no confirmation of that by external analyses.

Beyond sequencing problems, the software used to assemble and annotate the sequences may also be prone to errors in AT-rich and GC-rich regions. But many of those problems stem from the incompleteness of the sequencing.


Questions about the Evolution Theory I'm trying to understand more about evolution theory.
(I am coming from a mathematical background)

What i understand till now is that the "improvement" of the dna is a purely random development and the Selection criteria if the improvement was not negative is by surviving.

The better the improvment was the higher the likelyhood of surviving is.

What i don't understand is that the likelyhood that something useful comes from random changes in the dna is very low?

This reminds me of the http://en.wikipedia.org/wiki/Infinite_monkey_theorem it has surely a finite likelyhood but considering the complexity i still doesn't understand how for example wings of birds evolve.

Consider a pre-bird without wings, to get wings it has to have interstage with some useless pre-wings and then it has to learn how to flight.

Maybe someone can help me solve these mysteries :)

The other thing i am wondering is the smallest living element is the cell.
How did the first cell evolve?

Thank you very much

Welcome to BiologyBeta.SE!

On stackExchange sites, an OP should always limit his/her post to one question and should make his/her question is not too broad. But before you split up your question I invite you to have a look to some other post that will give you some answers. For this reason your question will very likely get closed as too broad. But I am giving some indices below. Also your post is a bit poorly written. This also lead people to close posts. Please come back with better posts, show some efforts in seeking for some information and it will be my pleasure to help you!

  Origin of life

There are already a bunch of posts on the origin of life for example. Note that the origin of life is not a field that is part of evolutionary biology as evolutionary biology only explain the evolution of life and not its origin. As a mathematician you may prefer saying something like the domain of definition of evolutionary biology does not include the origin of life just like the shannon's theory of information says nothing about the euclidian geometry.

  What i understand till now is that the "improvement" of the dna is a purely random development and the Selection criteria if the improvement was not negative is by surviving

Hum… that's sounds very weird. If I didn't know I would hardly recognize that you talk about evolution. You should have a look to some introduction to the field. Also, you should not confound the concepts of evolution, natural selection and mutations that I guess you confuse. A good, extremely simplistic view of evolution is that mutations occurs and create variance in the population. This traits are heritable. The variants that replicate the best increase in frequency in the population while the other variants will decrease in frequency up to the point to disappear. This is called natural selection.

  Consider a pre-bird without wings, to get wings it has to have interstage with some useless pre-wings and then it has to learn how to flight

You also seem to ask a question about how some traits may come to exist while what seem to be necessary intermediate would not be beneficial. This question has been answered probably a thousands of time as it is a common creationist argument.

Because your questions really sounds like creationist arguments I am a bit afraid that you are not trying to understand evolution but you wondering whether evolution does occur or not.

Note also that evolutionary biology is a very big field. You cannot expect to have a more or less good understanding of the whole science of evolutionary biology in less than a year. But if you are trying to just understand the very basic, sufficiently to persuade you that evolution does occur, then few weeks will probably be enough if you show some effort
Please don't forget the questions you may have. Seek by yourself for more knowledge and if you can't find something, then you're really welcome to come back to this site with an accurate question.

EDIT

Have a look to the definition of scientific theory. Also, please read @Chris comment below.

You misunderstand the meaning of "direct observation" that canadianer used. Observations we do in evolutionary biology are just as valid as those that has been made to confirm the theory of gravity. The only point concerns the easiness of understand these observations for non-literate in the field.

Yes, you are totally right. Just like the theory of gravity, the theory of evolution does not explain everything. It only applies to a subset of the phenomenons existing on earth. The theory of evolution is true, we know for a fact that evolution occurs but our theory is not global enough to explain things like the big bang or the surface tension and will never do so. The theory of evolution will never prove or disprove the existence of God as well (supposing you're concerned about that) because again it is not within its scope and will never be. However, the sociological impact of this theory tells much about the human behavior and our difficulties to accept something we know to be true if it contradicts some pre-establish believes even when these pre-established believes are not based on any logical developments.

Your question has been closed because it is too broad. The issue also is that your questions concern much more than evolutionary biology and biology. It also concerns the very nature of science and this is a common reason why creationist missundestand evolution. They don't (only) missunderstand evolution but they missunderstand what science is.