Do trees age on a microscopic level? Most animals age via at least two mechinisms:

at a "macroscopic" level, basically wear and tear to the point where (on evolutionary time scales) it's more genetically advantageous to optimize for reproduction rather than longer lifespans.
at a microscopic level, e.g. shrinking of telomeres. This prevents cell division after a certain point (good to prevent cancer and other growths, bad for regeneration).

Do plants also age microscopically? If so, how are we able to clone (in the horticultural sense) plants?

I've been doing some reading, and have come up with the following interesting information.

Telomeres

During cell division the DNA is replicated, but the mechanism is imperfect and in each round of cell division a small section is lost from the end of each chromosome. To compensate and protect the genetic information there are caps – regions of excess nucleotides – at the ends called telomeres (Silvestre, 2012).

Mammalian cells do not replenish their telomeres after cell division, giving them a replicative lifespan;  a maximum number of cell divisions before the telomeres run out. The cells then either enter a state of senescence and no longer divide, or initiate programmed cell death. However each cell has the genetic information for telomerase – the enzyme that can replenish the telomeres – but cannot use it. Only embryos and stem cells are able to express telomerase in mammalian cells - this protects against the build up of damage to DNA causing uncontrolled cell cycle progression. Activated telomerase is a core feature of many cancers (Campbell, 2012).

Plant Telomeres

You mention telomeres in your question, and it is an interesting question I had never considered. Plants have no germline preserved, so their progeny must bear all the defects of their particular parent cell, and that plant cells must therefore all have the capacity to regenerate their telomeres. I found a paper by Fajkus and colleagues that finds telomerase activity in plant cuttings grown in culture (Fajkus, 1998). Their hypothetical Plant Telomere-Length Regulating (PTLR) protein must arise in the early stages of the culture and last only a few cycles. Interestingly it seems that the efficiency of this process varies between different plant species. The authors note that their plant of choice – tobacco – is particularly proliferative and that other plants such as barley were harder to grow from cuttings, which may be down to a different way of regulating the telomerase (for instance it could only be activated occasionally at low amounts).

Do Plants Get Cancer?

It seems to me the next obvious question. One of the first papers I came across (published in 1916 by the Journal of Cancer Research!) talks of Crown Gall in plants and its relation to human cancer (Smith, 1916). Many websites cite galls as being the equivalent to cancer in plants, but it appears that the outgrowths (galls) that appear very tumour-like are in fact caused by bacteria encouraging their surrounding cells to proliferate. (See this question for more detail on galls).

I later found an abstract (I cannot access the full paper) from a paper published in Nature in 2010 called “Walls around tumours — why plants do not develop cancer” (Doonan, 2010). It appears that Plants can and do develop tumours, but they are less frequent and less lethal due to fundamental differences in development between plant and animal cells. Singh and colleagues found that in 2 plant species (Arabidopsis and rice) there were DNA damage repair pathways well conserved but with variation; there were several gene duplications in different DNA repair pathways (Singh, 2010).

Plants Do Not “Age” As We Do

Although I could find no conclusive evidence, it seems to me likely that plants may also have enhanced maintenance against other cellular stresses than DNA damage, such as build-ups of aberrant proteins. It therefore appears that in a protected environment some plants could live indefinitely. I say some, because others deliberately end their lives after reproduction. Traits such as longevity are inherently hard to be selected for, as the advantages come long after reproductive maturity and are therefore under much less selective pressure.

We see plants wither and die, but this is because they are constantly subject to environmental insult. Animals and insects may eat them, there may not be enough food or water, or sunlight, or the plant may become infected. All of which are at the macroscopic level. Due to completely different evolutionary constraints and pressures plants are highly resilient to cellar stresses, possibly due to differences in metabolic rate, and apparently have indefinite replicative potential.

Edit:
Although the more I think about it, the more it seems that most plant must have an ultimate lifespan, in that as they forever grow and expand their tissues would gradually harden and become less functional (I am mostly imagining bark plants here). Although as the layers of bark are pushed out the layers below take the place. In this way a tree could possibly live indefinitely by continuously remodelling it's layers.


What is the function of the Hyoepiglottic ligament? The hyoepiglottic ligament (ligamentum hyoepiglotticum) is an elastic band that connects the epiglottis to the hyoid bone.

Although I can find information about the clinical significance of this ligament (mentioned here), I have not been able to find a definitive or reputable description of its actual physiology/function.

Can anyone provide a reputably-supported description of the function (physiology) of the hyoepiglottic ligament?

My thought was that the hyoepiglottic ligament might act as a see-saw during swallowing. Specifically, my assumption was that as the hyoid is raised during swallowing (thus raising the hyo- end of the ligament), the opposite end of the hyoepiglottic ligament (attached to the epiglottis) is pushed down, forcing the epiglottis to cover the glottis to prevent food stuffs from getting into the trachea. Is this possibly right?

It's an interesting question. This 2010 paper contains some discussion of the function of the hyoepiglottic ligament. The following is a quote from the introduction:

  The epiglottis is connected to the
  hyoid bone by the hyoepiglottic ligament (ligamentum
  hyoepiglotticum), which is a connective tissue structure that
  serves as the roof of the paraglottic space and the
  preepiglottic space. Anatomically, the hyoepiglottic ligament
  separates the supraglottic larynx from the base of the
  tongue. Some clinical studies have shown that this
  ligament inhibits the spread and invasion of carcinoma... The hyoepiglottic ligament is elongated by
  approximation of the thyroid to the hyoid during swallowing.
  Tension on the ligament results in a “snap” retroversion
  of the epiglottis. Thus, the folded epiglottis represents a
  state of higher energy than that represented by the unfolded
  epiglottis; relaxation of the tension on the hyoepiglottic
  ligament releases the cartilage to automatically return to its
  normal resting position [emphasis mine].

In the study, the authors demonstrate histologically that the hyoepiglottic ligament is bipartite, with a part they call the pars hyoideus connecting the anterior epiglottis to the hyoid, and a part they call the pars lingualis connecting the epiglottis to the root of the tongue (they claim that this attachment to the tongue was previously unreported). Another quote from the paper follows:

  It is suggested that the pars lingualis plays an
  important role in active mechanisms such as upward
  movement of the epiglottis during phonation associated
  with tension of the lingual muscle and supraglottic airway
  patency during respiration.

To get some idea of how tension in a ligament anterior to the epiglottis can cause posterior movement (i.e. closure of the epiglottic 'flap'), I found this 1979 paper useful. They used cinefluorography to investigate the biomechanics of the epiglottis. The following lengthy quote should help to clarify the proposed model:

  The radiographic observations indicate that
  at the peak of the deglutitional excursion of the
  hyoid bone and the larynx the following circumstances
  prevail:

  (1) Forward translation of the hyoid bone in
  conjunction with extreme thyroid-hyoid approximation
  causes extreme elongation and
  tension on the hyo-epiglottic ligament at its attachment
  to the margins of the epiglottic
  tubercle.

  (2) The compression of the median thyrohyoid
  fold, secondary to extreme thyroidhyoid
  approximation, tends to make the epiglottic
  tubercle bulge backward transversely
  as well as vertically.

  The principle of the mechanism of folding
  deduced from these observations is demonstrated
  in a working model that can be set up
  in a few seconds. All that is needed is a rectangular
  piece of fairly stiff paper. The piece
  of paper represents the complete epiglottic
  cartilage (epiglottis and tubercle). A $\Lambda$-shaped
  crease is applied at the center (Fig. 4) to simulate
  the groove on the back of the cartilage,
  between the epiglottic tubercle below and the
  epiglottis proper above. One next applies stress to the model from the opposite side, at
  the site of attachment of the hyo-epiglottic
  ligament. This is done by grasping the paper
  lightly at the edges, below the level of the
  crease, whereupon the part above the crease,
  representing the epiglottis, immediately begins
  to fold down.
  Each limb of the crease functions as the
  directrix of a cone; the apex of the crease is
  the vertex of the cone. When the paper is
  gripped the directrices rotate towards each
  other and pull the attached paper after them,
  giving it a conical shape.

I've attached the figure 4 from the paper to illustrate better (I'm not sure if that's allowed on SE; please delete it if that's appropriate):

$\hskip 2 in$

The authors of this paper and this paper argue that the model just given does not fully explain the motion of the epiglottis during swallowing. The latter paper describes the existence of distinct lateral hyoepiglottic ligaments attaching to the ends of the greater horns of the hyoid bone. These, they argue, transmit the biomechanical forces generated by the movements of the hyoid and thyroid cartilage to the epiglottis to cause downfolding, although their full argument is too long to reproduce here.

Hopefully all of that has shed a little light on the possible function of this ligament. It seems to be quite complex, but there appears to be a relative consensus that the transmission of tension via this ligament is important in causing the folding down of the epiglottis during swallowing.


Difference of coverage between amplicons I have 2 fastq files and I generated BAM file (indexed and sorted) of some reads. I aligned them to a reference genome (hg19).

I am working with different primers.

FORWARD
1. TTGCCAGTTAACGTCTTCCTTCTCTCTCTG
2. CCCTTGTCTCTGTGTTCTTGTCCCCCCCA
3. TGATCTGTCCCTCACAGCAGGGTCTTCTCT
4. CACACTGACGTGCCTCTCCCTCCCTCCA

REVERSE
1. GAGAAAAGGTGGGCCTGAGGTTCAGAGCCA
2. CCCCACCAGACCATGAGAGGCCCTGCGGCC
3. TGACCTAAAGCCACCTCCTTA
4. CCGTATCTCCCTTCCCTGATTA

Therefore I have different amplicons. How can I plot the coverage of these different amplicons. And what could explain big difference between them?

Thank you very much for your help.

Well, to plot the coverage I would use something like Python Matplotlib. Take a look at this example:

import matplotlib.pyplot as plt
import matplotlib

amplicons =  ('TTGCCAGTTAACGTCTTCCTTCTCTCTCTG',
      'CCCTTGTCTCTGTGTTCTTGTCCCCCCCA',
      'TGATCTGTCCCTCACAGCAGGGTCTTCTCT',
      'CACACTGACGTGCCTCTCCCTCCCTCCA')
countAmpl = (1635, 4734, 2156, 3085)

fig = plt.figure(figsize=(10,8.5))

subplt = fig.add_subplot(111)
subplt.set_ylabel('Count')
subplt.set_xlabel('Amplicons')
subplt.plot(amplicons, countAmpl,  linestyle='-', marker='o', color='blue')
for tl in subplt.get_yticklabels():
    tl.set_color('blue')

plt.savefig("amplicons.eps")

Check other types of charts in Matplotlib if you think you need something else.

You can also try to open and visualize the BAM in IGV from the Broad Institute.

Regarding the difference in coverage, I would say that some are from a repetitive region. Or the amplification depth of a region is greater than for the others. Or maybe the aligner found similar regions and decided that the amplicon aligns well in all those regions.


Why does squinting allow you to see objects more clearly? How does squinting alllow one to see clearer pictures? What are the harmful effects?

This is an optical pinhole effect.  If the amount of light passed through the lens decreases, the sharper the image is at the focal point.  For a camera this is accomplished by increasing the f stop (f22 is a smaller aperture size than f6 — f-stop is an inverse number).  For the eye the iris will dilate (get larger) or contract to be smaller.  In very bright light, you can cut down on large amounts of light coming in by squinting, which creates a slit in front of the eye lens.

In photography this increases the "depth of field". Which is to say that more objects are in focus and sharp.  It works the same for our eyes of course.

In this image you can see as the aperture is smaller, any given point on the focal plane (right hand line) receives light from a smaller angle (i.e. from less of the image field).

I am not a physicist, but that's a first order explanation
@Luke reminds me that there was a question about whether squinting is harmful.  There is another reason that we squint.  If we are nearsighted or if we are getting older, we have a tendency to squint not because there is too much light coming into our eyes, but because our lenses are not focusing very well.  Is it harmful to strain our eyes?  Maybe, but it won't kill you.  Reading glasses won't either.


How can I predict DNA binding affinities from a protein sequence? Are there any computational tools to predict the binding affinity to specific DNA motifs from protein domain sequence information?

Those that come up from a Google search ("predict DNA binding from protein domain tool") seem pretty well suited to your question.

BindN
DNAbinder

Depending on your computational/statistical know-how you might also find these papers relevant

Huang et al, Predicting and analyzing DNA-binding domains using a systematic approach to identifying a set of informative physicochemical and biochemical properties
Gao et al, A threading-based method for the prediction of DNA-binding proteins with application to the human genome


Catching a cold outside in winter? We have all heard the typical “Put a jacket on youre going to catch a cold.” Usually stated by an older person typically a grandmother. Excuse the stereotype. Is there any evidence that colder weather makes one more prone to catching the flu or cold or is this simply a myth and misconception.

This is a pretty old old-wives tale, taking many forms: don't go out into the cold while it's raining, or without a hat, with wet hair, without a warm coat or scarf, without boots, etc., "or you'll catch your death of cold."

The old wive's tale was immortalized by Jane Austin in her book, Pride and Prejudice, when the heroine's sister Jane falls ill after getting a soaking in the rain.

This has been studied extensively. A New York Times article describes one such uncomfortable-sounding study:

  In the 1950's, Chicago researchers repeated the experiment on a larger scale with several hundred volunteers sitting in their socks and underwear in a 60-degree room before being inoculated with infectious mucus. Others, in coats, hats and gloves, spent two hours in a large freezer. The conclusion: all 253 chilled volunteers caught cold at exactly the same rate as 175 members of a warm control group.

In other words, being cold had no effect on catching a cold.

  A survey of the medical literature shows that for more than a century, scientists have invested an extraordinary amount of time and energy in debunking this old saw, with the aid of a small army of shivering, sneezing volunteers. But despite their efforts, the link between colds and the weather still lingers and continues to inspire yet more research.

A 1968 experiment studied the effect of (among other methods of chilling) a cold water bath at several stages during and after inoculation with rhinovirus (one of the many viruses responsible for the common cold). No effect.

Yet the studies continue, because anything shown to decrease the incidence of the common cold would be beneficial to the sufferers, as in the US alone, 75 to 100 million physician visits are due to the common cold, and millions of days are lost from school and work.

But what has never been proven is that getting chilled in any way causes one to come down with a cold.

There are a lot of studies that fail to show a corellation. However...
there are a handful of small studies that show that having cold and dry nasal mucosae increases the susceptibility of infection when inoculated with rhinovirus, though. So, if these studies are accurate, then being in the cold when exposed does increase the chance of becoming symptomatic.

'You'll Catch Your Death!' An Old Wives' Tale? Well...
Exposure to Cold Environment and Rhinovirus Common Cold — Failure to Demonstrate Effect
Acute cooling of the body surface and the common cold


Can you identify this species? It is similar to a kinkajou but it isn't for sure. I would include it into carnivora, and then maybe canifornia but I really don't have a clue.

That's a marsupial, the spotted cuscus, Spilocuscus maculatus.

Here is another image:

By the way, the same individual in your photo can be found in this site about Australian animals, still eating that starfruit:


DNA of the human body? If our DNA determines certain patterns within the human body such as hair color and eye color, if scientists were able to "turn off" such as the gene for eye color after the pattern was established, what would happen?

The classic analogy here is that of a blueprint. For example this one I found here which is kind of relevant:

If you use the blueprint above to make yourself a little sister and later change the blueprint, the sister you built will not be affected.

That is only part of the story though, the analogy can only go so far. DNA is constantly "read", what this means is that genes are transcribed to RNA which in turn is translated into proteins. To use a horrible simplification, genes are the blueprints for proteins. Therefore, if you change the gene, and the cell then reads from it to create a protein, it will indeed create a different protein than what the original gene would have coded for.

The point I am trying to make is that depending on which genes are changed, you can either have no effect or a huge one. Some genes are only read once when the cells are reproducing, others are read constantly as the proteins they code for are used up and then produced anew. So, if the gene you change is one that will be read again during the cell's lifetime, then you will see a change. A classic example of this is cancer. If, on the other hand, it is a gene that will not be read again, then the changes will not have any effect.


why didn't natives of south america evolve darker skin? I understand that darker skin tone is caused by melanin which helps to protect against the extra UV radiation that comes from more direct sunlight. It evolved in Africa before we migrated away from Africa and as I understand it was later evolved away from in areas further from the equator, where less sun meant less need for UV protection, because less sun also made it harder to get sufficient Vitamin D. Thus those near the equator tend to have darker skin and the further from the equator one goes the lighter the skin.

There are parts of South America which reside right on the equator, where melanin would provide important UV protection and where vitamin D deficiency was not a concern. I would expect them to have black skin, as dark as someone from Northern Africa or the Indonesians has, due to the extra UV exposure associated with the equator.

However, natives of Brazil and other equatorial parts of South America don't seem to have the same skin pigmentation as I see in the other equatorial areas.  They have skin darker then Europeans and other northern natives sure, but not to nearly the degree of other equatorial natives.  They clearly have the mutation for melanin, since that existed before we left Africa and they do have partial dark skin, which suggests that for some reason there was an evolutionary advantage to having skin as dark as theirs, but not darker.

Can anyone explain to me why South Americans wouldn't have evolved (or not evolved away from, depending on what part of the world they originated from) the almost-black level of dark skin the other equatorial natives possess?

Could not fit in a comment....

Northern Africans and Indonesians have pretty much the same skin color (to my first impression). Sub-Saharan African (that you don't talk about) are darker. And Northern Africa in not an equatorial region (not more than Los Angeles) as it is right under the tropic of cancer.

Also I am a little confused about who you call "we" and who call "they". I think that by "we", you mean any non-sub-Saharan African human but I am not sure. If this is the case just naming sounds more appropriate that to make a big category that you call "we" to exclude some ethnic groups :)

I think that when you are talking about Brazilians (and other people in South America living close to the equator such as Ecuadorians), you are mostly talking about people from Spanish and Portuguese descent. So let's talk about the great migrations

The Indonesians arrived in their lands about 70,000 years ago. The indigenous South-Americans arrived in South America about 10,000 years ago. The Spanish and Portuguese arrived in South America about 500 years ago.

I think you might want to read a bit more about the geography of those big migrations.


Why are prokaryotic promoter sequences written 5' to 3', when transcription proceeds from 3' to 5'? It seems that the promoter regions are written from the 5' to 3' direction. My lecture notes, for example, give the -35 and -10 promoter regions sequences like so:

Wikipedia seems to agree, on their article about promoters.

However, RNA polymerase transcribes in the 3' to 5', as in  it reads the template strand in the 3' to 5' direction. In that case, why aren't the promoter regions written also in the 3' to 5' direction?

Meaning, instead of the -10 sequence being 5'-TATAAT-3', why is it not 3'-ATATTA-5', in agreement with the direction of transcription?

My intuitive guess is that the $\sigma$ factor recognises the promoter region in a 5' to 3' directionality. But I cannot find any information to back up this guess. Additionally, if this is true, how could it have been determined (experimentally)? Furthermore, whatever the answer is, does it also apply to transcription in eukaryotes?

DNA sequence by convention is written starting at the 5' position so the directionality is assumed without explicitly writing the 5' and 3'. As for why its not the template strand sequence. I would say that's also a convention for simplicity because you only need to write one sequence if you want to discuss genes and regulatory elements.


Is Brain Eye connections reversed in all animals or just Humans? I know that Brain Eye connections are reversed in Humans,

Left Hemisphere controls the Right eye/Right side of the body
Right Hemisphere Controls the Left eye/Left side of the body

Is it true in other animals like Birds,Cephalopods and other creatures?
Are the optic nerves physically connected in reverse or is it internally mapped ?

That's not completely true. In mammals, including humans, the left of an image projects to the right of each of your retinae (this is due to the eye working like a camera obscura), and conversely for the right of an image. So you have 2 eyes, each eye receives mostly identical information but one is on the left and one is on the right of your body. You must somehow recombine this information together in the visual cortex. The way this is done is through the optic chiasma, where roughly half the nerves from the nasal parts (the half closer to the center of your body) of each retina cross. Then connect to a relay called Lateral Geniculate Nucleus and then connect to the brain. Below you can see a drawing from Ramón y Cajal, who first proposed this theory, depicting the process.

As you can see the points on each retina that receive information from the same parts of the visual field (here represented by the arrow) project to identical locations in the brain. So there is not a complete decussation (anatomical name for a crossing of nerves) like for muscles, but only a partial decussation of about half in humans.
Although y Cajal was the first to explain exactly why it makes sense to have partial decussation, this phenomenon had been known for a very long time. In facts Newton (hardly an anatomist) discusses that phenomenon in his Optiks and suggested that it might be related to the amount of overlap between the 2 eyes. So the more overlap, the higher the amount of partial decussation. This rule, later called Newton-Muller-Gudden law by Walls, seems to be approximately correct for mammals. However, as noted by Walls, there is no evidence of partial decussation in vertebrates other than mammals. Meaning that the decussation is complete (like muscles). In his Optiks Newton concludes that (I'm paraphrasing) if his theory is right then animals with no binocular overlap should have no decussation, which if he is well-informed is true for chameleons. His theory was indeed right but he was misinformed, chameleons have complete decussation.
Finally non-vertebrates do not have "contra-lateral" brains. They do not have this strange property of having each hemisphere mostly connected to the opposite side of their body. Therefore they have no decussation at all.
So in short: vertebrates-mammals = partial decussation ; vertebrates-non-mammals = total decussation ; non-vertebrates = no decussation.
Although dated, Walls book remain the most complete reference discussing decussation:
Walls, G. L. (1944). The vertebrate eye and its adaptive radiation.


What is the difference between fibrogenesis and fibrosis? Fibrosis is the formation of excess fibrous connective tissue in an organ or tissue in a reparative or reactive process.
I used the word "fibrogenesis" as the outcome of acute inflammation (healing).
My colleges use the word "fibrosis".
The fibrogenesis seems to be used with the emphasises of the genetic part.

What is the difference between fibrogenesis and fibrosis?

I would say fibrosis represents an abnormal accumulation of fibrous tissue usually collagen fibres. Where as fibrogenesis is the process of formation of fibrous tissues be it collagen, reticulin, elastic, oxytalan..


Gene Circuits; experiments First, my background - I'm a newcomer to biology.

What is a gene circuit, and how might I simulate one in a laboratory? Thank you.

I'm just going to give a broad idea of what a biological circuit is.  There's definitely more than one way to define them, but hopefully this will give you some idea.

Broadly, biological circuits are reminiscent of electrical circuits in that energy or information flows through the cell.  In biological pathways (a more typical terminology), genes in the cell (usually proteins) will use a signal (usually in the form of a chemical compound or a modification of a protein, but sometimes a simple ion or even electrical current (rarely)).  The signal then can be transmuted into a different chemical compound or it can even alter a protein so that it functions differently.

Here are a couple of classic examples.  The first is the Citric acid cycle (also called the Krebs cycle), discovered in the 1930s.  Here you can see that Citrate is chemically transformed into acetate and carbon dioxide and chemical energy in the form of NADH (reduced nicotinic acid dinucleotide).  Each step of the cycle has a different compound which is handled by a different protein enzyme.  While all the proteins and compounds may coexist in the same part of the cell, there is nonetheless an orderly circuit of chemical energy mediated by the genes of the cell and controlled by the cell as it adjusts the amount of enzymes available for each step of the cycle.

Another example of an entirely different sort of gene pathway works differently but has the same set of concepts.  Mitogen Activated Kinases (MAPKs) are proteins which have generally two states an activated state and an inactivated one.  As you can see below, an outside signal like high salt osmolarity or a signalling molecule is sensed by a receptor on the cell surface.  By some method a MAP Kinase is activated, perhaps by the addition of a phosphate to the surface of the protein or by dimerizing the MAPK.  Once activated, the MAPK will then phoshphorylate another kinase, which may activate yet another.  Finally a protein in the nucleus will be activated and cause transcription of some target genes.

In the latter case, a very small change to the protein costs little energy and information is being transmitted, but by biochemical signals where proteins are modified and affect other proteins.  That's a more subtle circuit than in the former case where relatively many individual molecules might be processed by enzymes together.

This hopefully gives you some idea of what a biological circuit looks like.  There are many other examples and subtle variations but that's a quick tour.

Experiments involving these pathways are too numerous to mention - individual proteins may be modified, their concentration within the cell can be altered by say mutations in the chromosome, pathway intermediate compounds like Succinate might be added to see how the citric acid cycle responds, isotopic labeled compounds can be added to see where they go in the cell.  There's nearly 100 years of experiments here.  that's a lot.

Hopefully this will just give you some idea of where to start.  Nearly any biochemistry textbook covers these topics in better detail, but then they are often over 1000 pages long!


Modern immunology textbooks I am looking for recommendations to good textbooks introducing modern immunology. Review articles, preferably modern (post 2000) would also be useful.

Please, include a brief comment with each book recommendation.

About book listing questions on SE: I understand that SE sites in general have adopted in the last year a policy against book listing questions. Instead, book lists should be moved to tag wikis. However, since BiologySE is still beta and young and the tag-wiki for immunology is mostly empty, I believe we would benefit from a question listing good introductory books to modern immunology, at least temporarily. Eventually, when Biology.SE matures, this question should be closed or locked, and the book recommendations herein moved to the tag-wiki for immunology. Moreover, for most other SE sites I have seen, the tag-wikis usually gather information that first appeared in questions like this, even if the question is eventually closed or locked. That's why I think this question will be useful to the community, at least temporarily.

I am surprised Janeway's Immunobiology is not listed here:

Murphy K. Janeway's Immunobiology. 8th ed. New York: Garland Science; 2011.

It is very comprehensive, accessible and goes beyond any graduate course I know. Most immunology researchers I know have a copy of this handy somewhere in their office. A particular highlight are the very clear illustration.

I would suspect that a new edition is currently in the works, so I recommend checking if a new edition is due to come out before you buy.


Which lipoprotein has the highest protein content? I know that HDLs have the highest protein/lipid ratio but know that the HDLs are very small molecules too and I couldn’t find the exact answer for this question. I mean, by amounts which of these lipoproteins have the most protein?

LDL has the higher protein content than HDL. LDL consists of Apo B48 and Apo B100. These are proteins with higher molecular weights between 250 kDa to 550 kDa as compared to other apoproteins. And these apoproteins are not present in HDL.

And if lipoprotein (a) is included in comparison then it has highest protein content.

(Via:  https://lipidmaps.org/resources/lipidweb/index.php?page=lipids/simple/lipoprot/index.htm)


What makes learning more difficult as we age? Why is it harder to adapt yourself to different cultures, places, and languages as you age? What makes breaking up with emotional patterns or ideas after years of habit more difficult?

Is there a natural process in which the neuron's synapses are set, while later in life the plasticity of the brain is nearly lost?

The answer(s) to this question can fill libraries. But I can give a few pointers here, as the question is relevant and timely, giving the tendency to an ever increasing life expectancy of the general populace in developed countries (notable exception: US).

I think your question can broadly be answered by the fact that degenerative processes in the brain slowly, but steadily, impairs all of its functions. Possible reasons for the specific decreased capability of the brain to adapt itself to new situations are:

The hippocampus plays a critical role in forming memory representations that are important for flexible cognition and social behavior (Rubin et al., 2014). Decreasing hippocampal neurogenesis during aging may impair the functioning of the hippocampus (Couillard-Despres et al., 2011)
Degenerative processes in the striatum impairs implicit learning that is necessary for mastering new tasks (Rieckmann & Bäckman, 2009);
Deficits in serotonin and dopamine neuromodulation in various brain structures due to degenerative processes during aging results in decreased learning and decision making (Eppinger et al., 2013);
Age-related altered neurosteroid levels may impair cognitive abilities (Vallée et al., 2011).

And the list goes on.

References
- Couillard-Despres et al., Gerontol (2011); 57: 559–64
- Eppinger et al., Ann N Y Acad Sci (2011); 1235: 1–17
- Rieckmann & Bäckman, Neuropsychol Rev (2009); 19(4): 490–503
- Rubin et al., Front Hum Neurosci (2014); 8: 742
- Vallée et al., Brain Res Rev (2001); 37(1–3): 301-312


What is the name of this plant has dazzling look like leaves? I am living in India. My neighbours are growing this plant and they even don't know what it was, but its leaves really dazzled me.

It is Jatropha podagrica also known as Buddha Belly.

It comes under succulent plants.

Source: flowersofindia.net


List of heritability estimates in humans? Many people on this site ask questions that directly or indirectly have to do with heritability in human.

Do you know a list of estimates of heritability of various traits in humans? Or could you try to create such list?

That might be great to have various kind of traits, personality traits, life-history traits, morphological traits, …

I am not necessarily asking for GWA studies that inform about what genes explain the observed variance (although that would be really great) but just some estimates of heritability and eventually information about the method used (parent-offspring regression, twins, ...) and which population was studied.

You may consider consulting the H2DB database. The database is quite new, so the number of heritability estimates is not very high at the moment (currently 225 estimates for human, 838 estimates in total), but it's a start. The database is described in a paper by Kaminuma et al.(2)


Breathing becomes harder in certain wind conditions I'm not sure if this is the right site to ask this, but it seemed like the best option.

I've observed on myself that, if I stand on a train platform and a cargo train drives by, creating strong, short gusts of wind, it becomes harder to breathe for me during the gusts, almost like fighting my body into breathing.

A commenton parenting.se leads me to believe this is due to the mammalian diving reflex.

1) is this assumption correct? 2) what causes the change in breathing?

So I'm going to go ahead and tell you outright that it is not the diving reflex.

What you are experiencing is the effect of air pressure.

Our lungs work off of pressure. Specifically our lungs inflate by using "negative pressure" (a word I've always hated). The pressure is not actually negative it is simply lower than the surroundings. Since there is less air in your lungs the air from the atmosphere rushes in because the pressure is higher outside your lungs. This is Boyle's Law (not the pressure outside being higher, but what happens when your lungs expand). Where an increase in Volume means a decrease in Pressure (if all else remains unchanged). In fact plants pull water up using negative pressure.

However to push out the air from our lungs we supply pressure using our muscles that overcomes the outside pressure and forces the air out.

The reason you feel your breathing change is because when that train passes by you correctly observed the strong gust of wind. This gust of wind has some force behind it that normally is not in the air you are breathing from the atmosphere. It has more force which increases the air's velocity. This actually decreases the pressure, but there's no need to get into that here (Bernoulli's).

The reason it feels like your body is "fighting to breath" is because the air is traveling in a direction with some force that you need to overcome by opening up your lungs just enough to "suck" the air in with negative pressure. This is more than the pressure you usually need to produce in order to breath in air that is "still".

What is funny to think about is we don't really have a muscle that "pulls" air in, even though it feels like you are actively doing that. The air actually rushes in on its own. All you do is expand your rib cage, which your lungs are attached to (look up on how, it's actually pretty cool), thereby making inhalation occur.

Now an interesting question for you to ask yourself is why is cold air harder to breathe?


Is a microspore diploid? In  gymnosperms the plant body is predominantly sporophytic. It produces microspores or megaspores my textbook says that these undergo reduction division in order to form male gametophytes pollen grains and female gametophytes that is egg.

The thought of a spore being diploid is revolting, as I have learned in the case of bryophytes and pteridophytes that it's haploid. Can anyone help me asap.

The spores (microspores or megaspores) in gymnosperms are haploid. The microspores came from the microsporocytes which are diploids cells of the sporophyte, divided via meiosis. So the haploid microspores do mitosis and form the male gametophytes (pollen grains), containing two male gametes (sperm cell) and a generative cell which will form the pollen tube.
The process conducting to female gametes in the ovule is very similar. A megasporocyte (diploid cell of the sporophyte) via two meiosis form four megaspores (haploid). Only one megaspore is functional (the others will degenerate) and do 3 consecutive mitosis to form eight nucleus with different functions, one of them is the egg cell (female gamete).
So the meiosis happens before the formation of the spores (actually it forms the spores) so they are haploid.
Source: R. F. Evert & S. E. Eichhorn "Raven Biology of Plants"


Is "TATA signal" synonymous with "TATA box"? In the text I'm translating I have a diagram of an expression vector. It has a lot of marks, and one says "TATA signal". I googled and found the expression "TATA box".

Are these expressions fully synonymous and interchangeable?

From Wikipedia:

  Considered to be the core promoter sequence, it is the binding site of either general transcription factors or histones (the binding of a transcription factor blocks the binding of a histone and vice versa) and is involved in the process of transcription by RNA polymerase.

So basically "TATA box" serves as a signal to the transcription machinery that says "transcribe this"?

"Box" is an archaic term from long ago. It's little used. "Signal" has now replaced it. "TATA box" and "TATA signal" are synonymous.


What species is this large-ish spider? Last night I came across this spider outside my house (costal Southern California). It was bigger than any I'd seen before, about 2.5 or maybe 3 inch legspan, maybe just under an inch for the body length. It is a brown-gray color, the cephalothorax has two dark brown stripes, and some mean looking fangs. Can anyone identify it?

Looking at this reference "Frequently synanthropic spiders of Southern California", I would have to say that it is possibly a grass spider. (Please someone correct me if I am wrong).

Beautiful looking specimen!


Why don't cells of aquatic animals burst? We know that if we keep plant cells in water, they don't burst because of a cell wall. But the cells of aquatic animals lack cell walls but they still survive. Why?

Comparative physiology of body fluid regulation in vertebrates

Cells are not passive components that always return to osmotic equilibrium. Through hormonal, cell signaling, and the number of pores for ion and water exchange marine animals can maintain osmoregulation in various aquatic environments. In land mammals osmoregulation is more passive since it is controlled by the endocrine system.


Coracoid vs. Coronoid - Etymology/Naming Choice? The word coracoid (e.g., coracoid process of scapula) literally means "resembling a crow/raven" or "of the form of a crow/raven." In this case, I assume, resembling the hooked characteristic of a corvid's beak.

Etymology: korax ("raven",Greek) + -oid (from Greek -oeidēs meaning "form").

However, the word coronoid (e.g., coronoid process of the ulna or of the mandible) also refers to a hooked projection of bone. Its etymology, however, is more straightforward:

Etymology: korōnē ("hooked", Greek) + -oid (from Greek -oeidēs meaning "form").

My question: Why the distinction?
 - Why is one termed the "coracoid" while the other structures are referred to as "coronoid"?

Since the coracoid process looks no more like an actual corvid's beak than the other structures, it seems that they should have all been referred to as "coranoid".

I get that we've just kept things the way they originally were b/c we like to do that in biology, but what was the original reason for the naming of the  coracoid to break from the trend?

It appears that both naming conventions originate with Galen, the Greek physician, almost 2000 years ago (for example, see: Singer, 1952).

Although the precise motivations behind the naming conventions aren't entirely clear, it seems that the origin of the coracoid naming convention is quite simple: Galen thought it looked specifically like a raven's beak, as you state, rather than the beak of some other bird.

Fortuine (2000) seems to suggest that the origins for both words originally applied to beaks of different birds, which implies that Galen may have thought some bone structures looked like beaks of one bird, and other bone structures looked like the beaks of another bird, so he used the corresponding terms of description. Specifically, "korōnē" may have referred to a crow or cormorant (I feel like the cormorant link makes more sense, though both are supported by Arnott (2007) - it may not be possible to know how the distinction was applied from surviving texts), as well as referring to a hooked shape. The same source mentions several other bird-derived terms, including the coccyx resembling the beak of a cuckoo and "rostrum" used more generally for beak-like structures.

Today, coronoid and coracoid may sound similar enough to be easily confused by students of medicine. However, giving these different bones distinct names does allow for some useful shorthand, such that one need not refer to the "coronoid of the scapula": I would assume, though I'm not sure if it is possible to find a good reference on this, that this is the motivation to keep things as-is, besides of course the history.

References

Arnott, W. G. (2007). Birds in the Ancient World from A to Z. Routledge, New York.

Duckworth, W. L. H., & Lyons, M. C. (2010). Galen on anatomical procedures: the later books. Cambridge University Press.

Fortuine, R. (2000). The words of medicine: sources, meanings, and delights. Charles C Thomas Publisher.

Singer, C. (1952). Galen's elementary course on bones.


Do you know what type of insect this is? I found these in my appartment (we live in a half basement). It's been three so far and I can't find the thing anywhere in insect lists, etc. Could you tell me what type of insect this is?

There are 900 different species of Crickets but I would say it is a Camel Cricket based on the info provided.


Can a single axon propagate multiple simultaneous action potentials? I have not been able to locate any research that indicates whether a single axon of a neuron or nerve cell can conduct multiple simultaneous (i.e. spatially separate) action potentials. I am aware that in many neurons refractory periods would preclude this possibility, however in some cases delays along axons are large enough.

Is this the case? Can you point me to any citations supporting your answer?

When you say multiple simultaneous action potentials I assume that the stimuli for all of them are temporally overlapping. In such case a neuron can integrate the different stimuli and launch an action potential. Of the multiple stimuli some can be excitatory while others can be inhibitory. The net response would be an integration of all the signals [ref].

However, if there is a gap in the stimuli then the cell may not react as it would be in its refractory period (which results until the ions levels are back to their original state and the membrane potential is restored).

There can be long delays, which depends on various factors such as ion deficiency, ATP deficiency (ATP is needed by Na+/K+ ATPase) or neuropathological conditions. In case of nervous signaling over many neurons then synapses can suffer from synaptic fatigue, which results because of depletion of neurotransmitters.

EDIT:

Maximum AP propagation speed/Nerve conduction velocity = ~120m/s (Can't find original source. From wikipedia)

Longest myelinated axon (sciatic nerve in humans) = ~ 1m

Time required to reach synapse = ~8ms

Time required for repolarization = ~5µs

So multiple action potentials (~160), are possible (lets call it situation-X).

The squid giant axon is ~500µm. I believe it is also non-myelinated. In this case if NCV is less than 100m/s then situation-X can happen. NCV can go as low as 0.5m/s (again the reference is wikipedia as I cannot find the original source).

Having said that, situation-X can also cause synaptic fatigue if the firing rate (AP frequency) goes beyond a certain value. This value would depend on how much neurotransmitter is released per AP, how much is in storage and the uptake rate.


Evolution of sexual reproduction from asexual How exactly did asexually reproducing organisms evolve into sexually reproducing ones? Why was it considered more favourable?

Sexual reproduction is a process where two cells fuse to form a diploid cell. Unicellular organisms (or even multicellular lower organisms like alga, fungi and protists) prefers to reproduce by asexual means under favourable conditions. But when the conditions become unfavourable, they opt to follow sexual reproduction. This suggests, sexual reproduction evolved to increase the chances of survival under unfavourable condition.

So how does sexual reproduction helps in increasing survival rate? By fusion of cells i.e., sexual reproduction a cell now becomes diploid and hence have two copies of its genome. This increased copy of genome is beneficial in repairing any breaks or alteration in genome, as the other copy will act as a template for repair (via homologous recombination).

To get a better hold of this, let us take an example. Let there be a population of haploid cells. This population was exposed to conditions which would cause damage to genome, specifically would cause breaks in DNA. There were two cells "Fella A" and "Fella B". They both knew that their genome has suffered damages, but neither was successful in repairing the DNA as they required an intact DNA template for repair. Suddenly "Fella B" came up with this great idea to fuse with "Fella A". This would work, reasoned "Fella B", as the position of damage in the DNA in his genome is different from the position in "Fella A". Fusion of cells was the first step towards evolution of sexual reproduction.

Later on the biological system realised importance of variation generated by sexual reproduction and hence this mode of reproduction caught on with various lineages.


How does translational coupling work in prokaryotes? Today I heard about a phenomenon called "translational coupling", where the translation of one protein influences the translation of another protein. The messenger RNA levels don't seem influenced. How does this work? Do they need to be in the same operon?

Translational coupling describes in how some cases an mRNA will code from more than one protein (i.e. will be polycistronic).  Translational coupling is thought to be mostly used as a way to make a set of genes are translated at roughly the same amount in the cell.

Translational coupling is very common in prokaryotes and nearly half of e coli genes are found in a polycistronic operon.  What we know about them is revealing.  There are some fancy mechanisms to adjust the ratios of these adjacent genes, which are still coupled, but with ratios that are not just 1:1.  Its shown that the later genes are often translated at somewhat lower frequency because the first genes are available more quickly before the mRNA degrades.

Eric Alm @ MIT wrote this great paper on how operons evolve.

I've only been able to find this reference to a eukaryotic case of "translational coupling" which is very rare, but does exist.  The most common cases of translationally coupled genes in eukaryotes are RNA viruses which usually contain only a single full length mRNA which codes for all the genes in the virus.  The selective pressures to keep the viral genome small and constrain the ratios of these genes, will cause these genes to even overlap, starting the next one before the current gene finishes.


1% water solution of deoxycholic acid. How is it prepared? According to Sigma, the solubility of deoxycholic acid is:

0.24 g/L in water at 15C

According to the FDA, Kybella (trademark) is a 1% water solution of deoxycholic acid.
How did they do this?

According to the sigma document you referenced (emphasis added by me):

"The free acid is soluble at 0.24 g/L in water at 15ºC, while the sodium salt is soluble at >333 g/L in water at 15ºC. Therefore, pH control is very important to the use of this product. Aqueous solutions precipitate as the pH is lowered to 5."

According to the FDA document (emphasis added by me):

"Each 2 mL vial of KYBELLA® (deoxycholic acid) injection contains 20 mg synthetic deoxycholic acid as the active ingredient and the following inactive ingredients: benzyl alcohol(18 mg), dibasic sodium phosphate (2.84 mg), sodium chloride (8.76 mg), sodium hydroxide(2.86 mg) in water for injection, USP. Hydrochloric acid and additional sodium hydroxide are added as necessary to adjust the formulation to pH 8.3."

The solubility of 0.24 g/L in water at 15ºC is determined by dissolution of the free acid in pure water. As you dissolve an acid in pure water, the pH will get progressively lower, and since this compound is less soluble at lower pH, it limits it's own solubility in pure water.
The sodium hydroxide in the KYBELLA is a strong base, which raises the pH and, when mixed with the deoxycholic acid, forms an aqueous sodium salt and water via an acid-base reaction. The conjugate base of deoxycholic acid in aqueous solution is deoxycholate. This portion of the compound remains unchanged, regardless if it is part of a free acid or a sodium salt. The sodium phosphate is a buffering compound which helps stabilize the pH and allows for finer adjustment to control the final pH to ensure it remains soluble.


Do plants have distinctive DNA genomes from each other like humans do? Can exact same species of plant have a distinct genome from others of same exact species growing nearby or in a different place/country etc. ?

Can a leaf be traced to the the exact plant based on DNA if we were to be given DNA of the "parent" plant of the leaf, and two test plants' DNA of exactly the same species?

Short answer: Yes!

Now for the longer answer. Yes, they do have distinct genes in general, but what you may see as different plants can also sometimes be clones. For example Quaking Aspen Trees which commonly grow in clonal colonies.

If you had a massive database of genetic material from plants you would be able to trace it. You may be able to, by doing sampling, work out where a sample was located geographically.


Gel electrophoresis after RNAse treatment I do not understand how to solve this question. I know that RNAse will cut smaller pieces of RNA.

The answer given is A

The question is a bit vague in some important parts, so I'll have to make a few assumptions about what the authors likely meant.

RNAses are enzymes that degrade RNA. There are a few different ones that lead to different kinds of degradation. The type that you would use in an experiment like this is an RNAse that completely degrades RNA. The purpose of this is to be able to distinguish RNA from DNA. So whatever is left after the RNAse treatment is DNA, and the bands that vanished are RNA.

If you isolate nucleic acids from liver, the major DNA part would be genomic DNA. The major RNA components would be mRNA and rRNA. Genomic DNA is huge compared to mRNA and rRNA. In gel electrophoresis of nucleic acids, the bands that move further are smaller nucleic acids, and the bands that move less far are larger nucleic acids. So the band on the left in your example is likely genomic DNA, and the band to the right is mRNA or rRNA. After RNAse digestion only the left band should remain, which is answer A.


"selective pressure" or "selection pressure"? Editing a manuscript of mine, a co-author changes "selection pressure" to "selective pressure". Are those two terms interchangeable? Or are there subtle differences that I'm not aware of?

The sentence under consideration: "In contrast, gene expression changes during development and tissue formation are under high selection/selective pressure."

FWIW, "selection pressure" is a bit more popular in the literature.

As far as online references are concerned, they should be equivalent (as "selective" becomes "making a selection"). The important difference in my understanding is that speaking in terms of biology, "selection" triggers associations with evolutionary terminology, whereas "selective" doesn't. Thus, as far as I am concerned, "selective pressure" could be referring to some machine that has a method of applying pressure to one thing but not another, whereas "selection pressure" immediately makes me think of factors benefitting the proliferation of one thing over another. Hence I would personally prefer "selection pressure".

Given the ambiguity, you probably won't be able to make all readers happy with either of the two. Thus, it might be best just to use a different phrasing as suggested e.g. by rg255 ("subject to selection").


Need of X or Y chromosome protein after meiosis After meiosis each spermatid get either the X chromosome or the Y chromosome. I know that the 4 spermatids formed from 1 spermatogonia are connected by cytoplasm and so the proteins made by X or Y chromosome can be shared by all the 4 cells.

I want to know what proteins made by X or Y chromosome are exclusive to the X or Y chromosome and are needed to convert spermatids to sperms.

X chromosome has many important genes required for general housekeeping. So we need not really talk about X-chromosome genes. Here is a list of genes present on the X-chromosome.

@Armatus, if all those genes were on autosomes then presence of Y wont be mandatory for male development. There are autosomal genes that are involved in sexual development for e.g. Anti-Mullerian Hormone gene is present on chromosome 19. However, there must be a master regulator that is male specific and since sex determination is chromosomal in mammals, the Y-chromosome must encode that master regulator.

Sry, encoded in Y-chromosome, is one such protein that is absolutely essential for male sexual development. Having said that, it could be very well possible that the basic genes required in the process of spermatogenesis are autosomally encoded. In fact it is so. I just took the list of genes that were associated with sepermatogenesis in KEGG and checked their chromosomal locations. They are all autosomal.

Gene --- position
SPATA1  ---  1p22.3
SPATA25  ---  20q13.12
SPATA32  ---  17q21.31
SPATA9  ---  5q15
SPATA19  ---  11q25
SOHLH1  ---  9q34.3
SPATC1L  ---  21q22.3
SPATA18  ---  4q12
SPATA2  ---  20q13.13
SPATA21  ---  1p36.13
SPATA2L  ---  16q24.3
GMCL1  ---  2p13.3
SPATA7  ---  14q31.3
SPATA5  ---  4q28.1
SPATA6L  ---  9p24.2
SPATA4  ---  4q34.2
SPATA24  ---  5q31.2
SPATS2L  ---  2q33.1
SPATA16  ---  3q26.31
SPATA6  ---  1p33
SPATA12  ---  3p14.3
SPATS1  ---  6p21.1
SPATC1  ---  8q24.3
SPATA22  ---  17p13.3
SOHLH2  ---  13q13.3
SPATA13  ---  13q12.12
SPATS2  ---  12q13.12
SPATA20  ---  17q21.33
ASUN  ---  12p11.23
SPATA8  ---  15q26.2
SPATA17  ---  1q41
SPATA3  ---  2q37.1
SPATA5L1  ---  15q21.1
GMCL1P1  ---  5q35.3
SPATA41  ---  15q26.3
SPATA42  ---  1p13.3
SPATA33  ---  16q24.3


Is chloroplasts per cell indicative of the photosynthetic power of a plant? Plant-A has on average N chloroplasts per cell. Plant-B has on average M chloroplasts per cell. If N > M, is plant-A more efficient in turning carbon dioxide into oxygen? Also, is it possible to see chloroplasts with a standard bright-field microscope?

You can say that but chloroplasts do not have uniform morphology across different species. Moreover some organisms such as red algae have chloroplasts of different origin.

Real indicator would be lets say number of chloroplast ATP synthases and/or light harvesting photosystems; these can be perhaps indirectly approximated by the total surface area of the thylakoids.

But for all practical purposes and comparison between not so distant species density of chloroplasts is a decent enough approximate for photosynthetic power.

About turning carbon dioxide to oxygen:

You should note that the source of oxygen is not CO2. Oxygen comes from photolysis of water; this is the initial step in the electron transport chain (ETC) in chloroplasts. The ETC results in production of ATP and NADPH; the latter is used in the Calvin-Benson cycle to fix CO2 to sugar.

So photosynthesis and carbon fixation, though associated in chloroplasts are basically different biochemical processes. Theoretically as long as NADPH is provided a plant should be able to fix CO2 [this is just my guess].

It is difficult to observe internal structure of chloroplasts with normal bright-field microscope but you can count them easily at 40x magnification. See here.


How do you visualize RNA on a gel? I have run an in vitro transcription reaction and produced some RNA of a single species and definite size. I would like to visualize it to check if the reaction worked.

Can I do this on an agarose gel? Is it sufficient to simply make a 1% TAE-agarose gel with EtBR that you would use for routine DNA electrophoresis, and run this? Is it necessary to take special measures against possible RNAses in the gel or the running buffer?

You have two possibilities: When you only need a quick check if your RNA is ok and you indeed only get one band, you can try a "quick and dirty" method. Heat the sample for 5 minutes at 65°C and then immediately cool it down in an icebath and keep it there until loading. By doing so, you melt up the secondary structure of the RNA and keep it in this state. You will most likely then see only one band.

If this doesn't work or if you want to use a RNA size marker, there is no way around denaturating gel electrophoresis. Here you denature your sample in the loading buffer and then run a denaturating gel in which prevents the secondary structures. There is a good paper about this:

Denaturing RNA electrophoresis in TAE agarose gels

The classical method using formaldehyde (which is more dangerous in handling) is described in the following paper and also in the "Molecular Cloning: A Laboratory Manual" book by Maniatis and colleagues:

RNA molecular weight determinations by gel electrophoresis under
denaturing conditions, a critical reexamination


Linkage disequilibrium I want to know what ranges of value can D' in linkage disequilibrium take? Because I read in my book (An introduction to population genetics by Nielsen and Slatkin) that D' is guaranteed to be between 0 and 1. Whereas at the link provided below, it says D' can be between -1 and 1.

http://csg.sph.umich.edu/abecasis/class/666.03.pdf

Could someone explain this discrepancy? Because now I am totally confused.

The whole point about using D' rather than D is because D' is bounded between -1 an 1 for any allele frequency, while the bounds for D depends upon the allele frequency of interest.

Recall the definition of D

$$D = p_{ab} - p_ap_b$$

Let, $D_{min}$ and $D_{max}$ be the minimal and maximal values of $D$ for a specific allele frequency.

For $p_a = p_b = 0.5$, the  $D_min$ is when when $p_{ab} = 0$ ($D_{min} = -0.25$) and $D_{max}$ is when $p_{ab} = 1$ ($D_{max}=0.75$).

For $p_a = 0.8$ and  $p_b = 0.2$, the  $D_min$ is when when $p_{ab} = 0$ ($D_{min} = -0.16$) and $D_{max}$ is when $p_{ab} = 0.2$ ($D_{max}=0.04$).


Pen and paper game to explain the theory of evolution Sometimes when explaining the theory of evolution one sees a glazed-over look on the persons face. To this person the theory seems completely incomprehensible no matter which avenue one takes to explain it. This leads me to think that a game might be a fun alternative. In the process of playing, I suspect that the player might pick up a stronger intuition of how and why it works which would eventually lead to understanding the basics as a whole.

It is easy enough to dream up any number of problems that can be presented as a genetic algorithm with pen and paper, the challenge however is to make it easy to understand and fun to play.
Does anyone know of such a game or able to construct such a game?

Not sure if this qualifies as pen-and-paper, but one game I am familiar with to highlight natural selection goes something like this:

Materials:

Creatures - Small paper pieces of different colors from construction paper - hole-punch remnants work great, or you could cut squares

"Habitats" - Large, colorful surfaces. Whimsical maps work well for this, maybe certain posters, the important thing is to have some diversity.

Gameplay:

This is ideally done in multiple groups, each group should start with an equal ratio of creatures of at least two different colors.

One or more people spread the Creatures around the Habitat.

Another student (or multiple) act as the "predators". They sit/stand above the board and close their eyes; then they open their eyes, and harvest the first Creature they see. Close eyes again, and repeat until 1/2 of the Creatures have been eaten.

Count up the paper pieces and note the number of each remaining; for the next Generation, the Creature makeup should be 2X the number of remaining pieces: so if there are 30 Blue and 20 Red remaining, the new generation is 60 Blue and 40 Red.

Repeat over a few generations - the result should be that different habitats lead to different proportions. You can also change things up by suddenly shifting the habitat!

You could possibly include genotypes and recessive traits for an older group (the version I suggested is effectively haploid parthenogenesis), these might be harder to keep track of.

(I don't have a citation for this game but if anyone knows it, please provide in the comments!)


What could make a person get ill from not eating often enough? Say a person needs to eat every 3 hours, or s\he gets physically ill with fatigue and cold sweating, and this is the case every day.

What could cause this?

This could be a symptom of hypogylcemia.

Hypoglycemia causes symptoms such as:

hunger
shakiness
nervousness
sweating
dizziness or light-headedness
sleepiness
confusion
difficulty speaking
anxiety
weakness


Apparent paradox in Glucagon action Glucagon stimulates glycogenolysis and gluconeogenesis, thus increasing the plasma glucose concentration — so that tissues get enough glucose in the fasting state.
However glucagon also inhibits glycolysis. In this case, what is the point of having high blood glucose if it cannot be catabolized?

Summary
The apparent paradox is resolved by the fact that not all tissues possess receptors that cause them to respond to glucagon or, more generally, to the same hormone. Where different tissues do respond to the same hormone, the tissue response may differ because of differences between the pathways or particular enzymes within the different tissues. Tissues that use glucose in starvation generally do not have glucagon receptors. In the related situation of response to epinephrine, the glucose utilizing tissue, skeletal muscle, does not contain the particular enzyme isoform that is subject to cyclic AMP-dependent control in liver.
General principles of hormone action in the regulation of metabolism
Metabolism in simple, especially unicellular, organisms is regulated by supply and demand. The mechanisms underlying this are mass action and allosteric activation or inhibition of key enzymes. In more highly developed organisms with differentiated tissues serving specialized functions there are times when this intercellular control must be over-ridden to produce an integrated response to the overall benefit of the organism. This is the rationale for hormonal control.
An integrated response does not mean that each tissue responds in the same way. It means that each tissue responds in a manner that is appropriate for the organism as a whole, given the function of the tissue and its priority (e.g. for rationing of energy sources). A simplified example of how this is achieved is illustrated below.

Tissues 1 and 2 (e.g. liver and skeletal muscle) both contain pathway P1 (e.g. glycogen degradation), but only Tissue 1 responds to hormone H1 (e.g. glucagon) because Tissue 2 does not have the receptor R1, for H1. (SM is the second messenger involved in the signalling, e.g. cyclic AMP.)
Tissue 2 (e.g. adipose tissue) does have the receptor for hormone H1, but responds in a different way because it lacks pathways P1 and P2 of Tissue 1, but contains a tissue-specific pathway P3 (e.g. triglyceride breakdown).
Hormone H2 (e.g. epinephrine/adrenalin) affects Tissue 2 (e.g. skeletal muscle) as well as Tissue 1 (and 3), but the response is only partially similar in that although they share pathway P1, Tissue 2 lacks pathway P2 (e.g. gluconeogenesis).
Differential response to glucagon
Put simply, glucagon is a signal for starvation. Hence the appropriate integrated response is for those tissues (liver and adipose tissue) that can supply energy sources (glucose and fatty acids, respectively), and those tissues with greatest need for the scarcest resource (brain with its requirement for glucose) are supplied it, while those tissues that can manage with the alternative (fatty acid) are made to use it instead.
The brain has no receptors for glucagon (or insulin), so it can utilize the glucose made available by the liver. (Likewise the erythrocytes.)  The main factor preventing other tissues using glucose is that they have insulin-sensitive glucose transporters and the blood concentration of insulin drops in starvation. It is only liver where there is need to make sure that the glucose produced by gluconeogenesis is not glycolyzed.
But doesn’t the paradox remain if we consider epinephrine?
The function of epinephrine is to initiate the ‘fight or flight response’, which involves supplying energy metabolites for skeletal muscle contraction. This involves both the liver, which breaks down glycogen to supply glucose to the muscle through the blood, and the skeletal muscle itself, which breaks down its own stored glycogen. As epinephrine also acts through cyclic AMP, which inhibits glycolysis in liver, why is glycolysis not inhibited in skeletal muscle?
The answer to this is that cyclic AMP inhibits glycolysis by phosphorylating and activating the liver enzyme PFK2, which catalyses the formation of fructose 2,6-bisphosphate, an allosteric activator of phosphofructokinase. Skeletal muscle has a different form of FPK2 which is not affected by cyclic AMP, lacking the regulatory phosphorylation sites. (It is regulated by other metabolites.) Hence in liver, glycogen, through cyclic AMP, causes the concentration of fructose 2,6-bisphosphate to decline and, thus, the activity of phosphofructokinase (PFK) to be decreased, preventing glycolysis; whereas in muscle the concentration of fructose 2,6-bisphosphate does not change.

This regulation of phosphofructokinase by fructose 2,6-bisphosphate is described in sections 16.2.2 and 16.4 of Berg et al. (although they seem to have forgotten about skeletal muscle). However as the overall mechanism and details are somewhat complex, I have produced a simplified summary diagram of my own, above, in which the green lines indicate activation, and the red lines inhibition.


GATK workflow for Cancer I am just starting to learn to use bioinformatics tools.  My university has a limited and expensive bioinformatics team, so I'm mostly on my own except for big questions.

I am planning to use GATK to run 58 cancer control/normal pairs of Exome sequencing data (Illumina) from FASTQ or BAM file format, through the pipeline, with an output of a VCF & MAF format for analysis.

The current GATK pipeline is used for disease but not cancer, so I was wondering if anyone knew if there should be changes made for cancer.  Here's the current pipeline starting with BAM files:

(Non-GATK) Picard Mark Duplicates or Samtools roundup
Indel Realignment (Realigner TargetCreator + Indel Realigner)
Base Quality Score Reacalibration (Base Recalibrator + PrintReads)
HaplotypeCaller
VQSR (VariantRecalibrator and ApplyRecalibrator in SNP and INDEL mode)
Annotation using Oncotator (?)

I'd like some verification that this pipeline will output what I need to run my samples on MuTect, MutSig, or some other analysis program.  I appreciate any advice.

This post goes over what MuTec requires as input. mark duplicates and indel realignment will probably have to be done on bam file to use it as input. BQSR is optional and does not change the quality too much. HaplotypeCaller is used for germline not somatic variant calling.

If you have followup bioinformatics questions, you might be able to find answers more quickly on biostars or GATK forums


Understanding the strategy of Sanger DNA sequencing The Sanger sequencing method creates large numbers of sequences of all possible lengths, ending with a specific nucleotide, by terminating with a tagged (fluorescent) nucleotide at the end.

But if you already have fluorescent nucleotides of a specific base, why not just do regular PCR  with them, create a huge number of full length copies of the original sequence, and then simply see the locations where the nucleotide fluoresces to determine all the locations of that base. Why do we need a large number of copies ending at each possible location, as with the Sanger method?

If you mark the full length strand of the DNA with the fluorescent labels, you will get a lot of signals from the same nucleotide without the possibility to discriminate where the actual nucleotide is located on the strand.

Sanger sequencing doesn't end with the preparation of the terminated and labelled DNA strands, the following step is crucial in discriminating where the labelled base actually is. After labelling, the sample is run through high resolution capillary gel electrophoresis to sort them by size. The smallest fragment comes out first, then the one with one base more and so on. The detector which then identifies which fragment is coming through is located at the end of the capillary.

This works like shown in the schematic image (from here):

If you would mark a complete strand, no dicrimination by size is possible (ideally, all DNA would run on the same height of a gel) and all flourescent signals for all positions would come on the same spot. Not very helpful.


New earliest life found, what are the implications? So a couple of days ago it was announced that new fossils of microorganisms were possibly discovered around former hydrothermal vents. According to the paper these fossils "are at least 3,770 million and possibly 4,280 million years old" making them the earliest instance of life found so far. If the upper estimate is correct that would mean these organisms existed "only" ~250 million years after the formation of Earth.

Does this discovery shake up any of our previous ideas and/or provide new insights about the earliest life?

Not a lot, the sample is not conclusively biotic in origin nor is it necessarily much older than known fossils, 3.7 billion vs 3.5 billion. The sample is a few simple hematite filaments, complex hematite filaments do form as a byproduct of oxygen using (aerobic) bacteria, they can also be formed by metamorphic processes. Subscribing these filaments to life and proposing oxygen must have been present far earlier than any evidence supports based on this is wishful thinking at best.

If it were correctly identified and as old as possible it would have only a small effect, it would make finding life on other planets more likely becasue it would mean life forms basically as soon as you have persistent liquid water. It might indicate oxygen earlier than suspected but that seems unlikely.


"structural and regulatory elements of genes" Can anyone please explain a little about these two elements of genes? My main problem is with "which ‘switch on’ instructions".

  genes have structural elements (which code for a particular protein) and regulatory elements (which ‘switch on’ instructions)

The expression of protein coding genes happens by the process of transcription. So promoters facilitate access of the RNA polymerase complex to DNA to begin transcribing a locus on the genome. The promoter of a gene often contains sequences that bind proteins called transcription factors, which play a role in various parts of the transcriptional process as well as components of RNA polymerase themselves (Such as a Pribnow box in prokaryotes, or a TATA box or an initiator element in animals).

So whether a gene is turned on and if so, how much it is turned on, is a property of how many transcription factor binding sites exist in the promoter, the nature of the transcription factors themselves in terms of their influence on transcription, and in eukaryotes and some archaea, epigenetic processes that control the access of transcriptional machinery to the locus being transcribed.

So when you think about the two elements in a gene, think of a light (the bit of a gene that codes for proteins) and a dimmer (which controls how much RNA is made by the protein-coding bit)


What is the mechanism of folic acid deficiency and neural tube defects? I am having difficulty finding the mechanism by which folic acid reduces the risk of neural tube defects. I know that it does so, but what in particular actually occurs with folic acid deficiency to cause the neural tube defect? Is that completely unknown and merely a strong association, or is there a putative mechanism?

You are having difficulties finding the mechanism because it is as of yet unknown.

Now of course comes the hard part where I need to prove that statement. Often, it's just apparent by papers not saying anything about the mechanism, even though you'd expect then to include a brief section if it was known, for example Folic acid supplementation for pregnant women and those planning pregnancy: 2015 update or the various Cochrane reviews on the topic of how much folic acid supplementation is optimal, or the WHO and CDC documents on the topic

Here's a few relatively recent ones that state it outright:

Folic Acid Supplementation and Pregnancy: More Than Just Neural Tube Defect Prevention, 2011

  The mechanism by which folic acid prevents structural anomalies in the fetus is not known, but may involve the regulation of homocysteine metabolism

Folic acid supplementation in pregnancy and implications in health and disease, 2014

  as FA deficiency may be a risk factor for NTDs additional studies will be required to determine the mechanistic role of the FA pathway in the onset of neural tube defects

FA = Folic Acid, NTD = Neural Tube Defects

Neural Tube Defects, Folic Acid and Methylation, 2013

  To date, animal studies have not provided
  sufficient information to establish the metabolic and/or genomic mechanism(s) underlying human folic acid responsiveness in NTDs.

There are some putative mechanisms to do with folic acids effects on the homocysteine metabolism and its effects on methylation. I can't really tell how well-established those are yet, but maybe this can be a starting point for you.


will an earthworm survive after covering its skin with a wet cloth I am very curious about this question. I got this doubt when I was studying anatomy and physiology of the earthworm Lampito mauritii. It breathes through its skin (cutaneous respiration) and if we cover its body with a wet cloth and all the necessary external openings are left uncovered (such as nephridia and other genital pores) then will the earthworm survive?

This is one of those speculative questions where you don't have a definite answer unless you specifically experiment and find out for yourself.

It is a known fact that earthworms breathe through diffusion. It has a thin cuticle over its body and requires moist skin which is achieved by a slimy mucous (reference). It is interesting to note that earthworms are also capable of going into a state of hibernation called estivation (in American english) (reference) which helps them maintain a low metabolic state.

Since you are planning to cover it with a cloth, the material of the cloth also matters. It has to be a material with low breathability. For eg: the survivability of the worm would depend on if you were using a wool or a silk cloth to cover it. Here is an article on the breathability of different fabrics (reference).

In conclusion, I would take a guess that it should survive if the material let air pass through and would go into a state of estivation on low availability of oxygen but maybe not die. After all, they are said to be able to survive even in water  if it contains enough available oxygen. (reference).


What is the length of gene when calculating TPM (transcripts per million) What is the length of gene when calculating TPM (transcripts per million)?
Assume I have a dataset matrix with k rows(each row is a gene) and n columns (each column is a sample), is there any way I could transfer the data set into TPM? Many thanks!

Assume we have

$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & 10 & 15 & 30 \\ B\: (5kb) & 25 & 25 & 70 \\C\: (2kb) & 6 & 10 & 17 \\D\: (8kb) & 1 & 1 & 3 \end{bmatrix} \: \:$$

To transform this into TPM format, we need to normalize for gene length, and then normalize for gene depth, in that order.

Normalizing for gene length..

Step(s) To Perform: Divide each replicate count by the length of its respective gene.

For $Gene A$, it has a length of $2kb$ (kilobases), with replicate counts $10, 15,$ and $30$. Performing this operation on the entire table,

$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & \frac{10}{2} & \frac{15}{2} & \frac{30}{2} \\ B\: (5kb) & \frac{25}{5} & \frac{25}{5} & \frac{70}{5} \\C\: (2kb) & \frac{6}{2} & \frac{10}{2} & \frac{17}{2} \\D\: (8kb) & \frac{1}{8} & \frac{1}{8} & \frac{3}{8} \end{bmatrix} \: \:$$

yields

$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & 5 & 7.5 & 15 \\ B\: (5kb) & 5 & 5 & 35 \\C\: (2kb) & 3 & 5 & 8.5 \\D\: (8kb) & .125 & .125 & .375 \end{bmatrix} \: \:$$

Normalizing for gene depth..

Step(s) To Perform: 1) Sum all counts within each replicate column; 2) Divide each column sum by the desired depth (this yields scaling factors); 3) Divide each replicate count within a column by its respective scaling factor.

$Rep1$

Sum: $5 + 5 + 3 + .125 = 13.125$
Scaling Factor:  $\frac{13.125}{1,000,000} = 1.325 \times 10^{-5}$

$Rep2$

Sum: $7.5 + 5 + 5 + .125 = 17.625$
Scaling Factor: $\frac{17.625}{1,000,000} = 1.7625 \times 10^{-5}$

$Rep3$

Sum: $15 + 35 + 8.5 + .375 = 58.875$
Scaling Factor: $\frac{13.125}{1,000,000} = 5.8875 \times 10^{-5}$

Applying these values to the table,

$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & \frac{5}{1.325 \times 10^{-5}} & \frac{7.5}{1.7625 \times 10^{-5}} & \frac{15}{5.8875 \times 10^{-5}} \\ B\: (5kb) & \frac{5}{1.325 \times 10^{-5}} & \frac{5}{1.7625 \times 10^{-5}} & \frac{35}{5.8875 \times 10^{-5}} \\C\: (2kb) & \frac{3}{1.325 \times 10^{-5}} & \frac{5}{1.7625 \times 10^{-5}} & \frac{8.5}{5.8875 \times 10^{-5}} \\ D\: (8kb) & \frac{.125}{1.325 \times 10^{-5}} & \frac{.125}{1.7625 \times 10^{-5}} & \frac{.375}{5.8875 \times 10^{-5}} \end{bmatrix} \: \: $$

yields

$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & 377358.49 & 425531.91 & 254777.07 \\ B\: (5kb) & 377358.49 & 283687.94 & 594479.83 \\C\: (2kb) & 226415.09 & 283687.94 & 144373.67 \\ D\: (8kb) & 9433.96 & 7092.20 & 6369.43 \end{bmatrix} \: \:$$

The dataset is now TPM formatted, which offers an easier analysis of read proportions throughout the sample.


Why is thymine rather than uracil used in DNA? What is the advantage gained by the substitution of thymine for uracil in DNA?  I have read previously that it is due to thymine being "better protected" and therefore more suited to the storage role of DNA, which seems fine in theory, but why does the addition of a simple methyl group make the base more well protected?

One major problem with using uracil as a base is that cytosine can be deaminated, which converts it into uracil. This is not a rare reaction; it happens around 100 times per cell, per day. This is no major problem when using thymine, as the cell can easily recognize that the uracil doesn't belong there and can repair it by substituting it by a cytosine again.

There is an enzyme, uracil DNA glycosylase, that does exactly that; it excises uracil bases from double-stranded DNA. It can safely do that as uracil is not supposed to be present in the DNA and has to be the result of a base modification.

Now, if we would use uracil in DNA it would not be so easy to decide how to repair that error. It would prevent the usage of this important repair pathway.

The inability to repair such damage doesn't matter for RNA as the mRNA is comparatively short-lived and any potential errors don't lead to any lasting damage. It matters a lot for DNA as the errors are continued through every replication. Now, this explains why there is an advantage to using thymine in DNA, it doesn't explain why RNA uses uracil. I'd guess it just evolved that way and there was no significant drawback that could be selected against, but there might be a better reason (more difficult biosynthesis of thymine, maybe?).

You'll find a bit more information on that in "Molecular Biology of the Cell" from Bruce Alberts et al. in the chapter about DNA repair (from page 267 on in the 4th edition).


Detecting Calcified stones and cracks in tooth I had a dental problem when my first molar broke some months ago and after some decay and pain I am undergoing a dental treatment. The doctor was performing a root canal and kept on talking about calcified stones being formed and looking for a 'tak' sound inspite of having x-rays. Doctor did not point to the calcified stones earlier and suddenly came out with this new issue. In the mean time when looking for stones doctor actually managed to break my tooth and has blamed grinding and clenching for a crack that caused the tooth to break.

I am shocked that neither the calcified stone nor the crack showed up in x-ray and the preliminary examination. With current technology, can the cracks in tooth and calcified stones not be detected.

Cracks on your teeth are hard to detect if they are cracks on the mesial or distal surfaces (surface of the tooth closest to and farthest from the midline respectively) through x-rays. Please check this link for illustrations and very good explanations from the University of Maryland dentistry department. The different methods on the detection of cracks as well as the uses of radiographic evidence can be found in this link.

Now pulp stones can be identified through x-rays unless they are too small or not too dense. There has been researches done specifically using radiographs for detection like "A radiographic assessment of the prevalence of pulp stones in Australians". It could also be human error that your doctor was unable to detect it. A small explanation on pulp stones can be found here.


What is the most common way of administering loop diuretics and what is their time course of action? I am reviewing some material on loop diuretics, and I am curious to know how these drugs are administered. Also, I am interested in knowing their time course of action once they are administered into the body.

I know that furosemide (there are more types of loop diuretics) can be given intravenously (but can be orally given as well (furosemide info sheet)). Effects of i.v. furosemide are pretty much immediate as it is carried quickly to the kidneys via the blood. After i.v. administration the effects wear off in about half an hour. t1/2 is about 2 hours, but likely depending on route of administration.


Why our bees might have suddenly disappeared We have a large garden in Bedfordshire, UK, next to woods and to arable fields currently planted with intensively farmed rape. We usually have many bees in the garden. Earlier this year, things were humming along as usual. A cotoneaster bush in flower had perhaps a hundred bees on it at once, of at least 6 different species.

Now, in July, we have lavender and clover in full bloom, normally swarming with bees. But, not now. This morning (overcast and warm) there were two bees on a lavender bush covering two square metres. I can walk for minutes in the garden without seeing a single bee. The leafcutter bees have left no holes in our rose leaves this year.

The nearest managed hives are about 800m away. It's not just a managed hive that has gone, the bumblebees that nest in our garden have gone too.

The rape flowers are long past. I don't know what might have been sprayed on the rape.  Our garden is organic.

Wasps are down too. This is the first year in the last twenty that there are no wasp nests in our outbuildings. There are, however, plenty of flies.

What might have caused such a sudden and unusual population change? Among multiple species of bee from multiple sources, between April and July?

Could it be our globally-warmed weather? June and July have been wetter and warmer than usual, although not exceptionally so.

Are UK farmers allowed to use an insecticide on rape that could kill most bees?

Or is a dramatic in-year population change in bees a routine, if uncommon, event?

Thanks!

Update August 17 2016

Our garden bees do seem to be gradually recovering - nothing like most years, but a few bees are coming back. Other nearby houses, at least 400m from the nearest rape field, have plenty of bees.

We call it Colony Collapse Disorder (CCD).

Consequences

The phenomenon is observed worldwide and is pretty serious. Northern Ireland lost 50% of its beehives for example. Between 1997 and 2003, 10 millions beehives were lost. Many cultivated crops are pollinated by bees and we don't quite have an alternative today. In 2005 a study showed that the worth of crops that are pollinated by bees is around 200 billions dollars.

Causes

Why? The short answer is "we don't know". There are a number of possible factors and the general consensus is to think that there is not a single factor that is causing the decline but it is a combination of different factors. Possible factors include:

Pesticides
Pathogens
Fungicides
Antibiotics
Miticides
Climate Change
migratory beekeeping
loss of genetic diversity through too intense selective breeeding
malnutrition
parasitic phlorid fly

More information

The wikipedia article for CCD is very complete. You should have a look at it!


Drinking River Water Unsafe? I've read that drinking river water is unsafe. Did people in the past drink water from the well exclusively or did they deal with diarrhea constantly?

It very much depends on the river and location along that river. if there is a city upstream who is defecating into the river, you'd better not drink from that river. But drinking from the same river upstream of this city could be totally fine.

Disease transmitted through the faeces were very common in the the 19th century especially in cities that had no system of evacuation of wastes. Now, of course the prevalence of such diseases depends on the type of society and therefore on the era and location.

Generally speaking, it is always best to carry tap water (or bottled water) on you. If you have to drink from a river, be cautious, talk to local people, think of what could live upstream (people, cattle, ...) and always use a good filtration system before drinking from any river.


What bird species is this? (Heron-like waterfowl from China) I need help identifying this bird.  (Some sort of heron?)

It was seen in Wuhan, Hubei, China, in September.

It is very common there.  It can also swim like a duck, but I've only seen it do this once (it's not something they commonly do).  I can supply more photos upon request.

These are two different individuals:

I'd go with juvenile striated heron. I ruled out others such as the chinese pond heron because of the spotted wing plumage and slightly different shape of the patch around the eye. The night heron seems to have a more red eye than the striated heron and appears to have a stubbier beak.

Arkive is a good place to see a lot of pictures of birds, this is a good birding site, and otherwise I use generic google searching (e.g. start with "herons china" or "herons asia") - this at least helps narrow down the search quite substantially and is considerably cheaper than having a library of the worlds bird books!


Calculation of saturation of carbon in surface waters I've been looking at some journals lately that look at carbon emission from lakes where some lakes act as sources and other act as sinks. The paper that I have been looking at is

http://www3.nd.edu/~underc/east/publications/documents/Cole_94Science.pdf

where they show that lakes are sources of CO2 to the atmosphere. What are the equations that are used to determine the saturation of CO2 in surface waters?

The recent IPCC report also mentions that lakes act as sources of CO2 but does not give any indication of the equations used to come up with these values. Presumably, to determine the concentration of carbon in the surface water you need to use other measured variables such as temperature. Can anyone suggest a method for estimating this concentration ?

Take a look at Paragraph 2.

I'll outline it in more or less plain english (I hope).

for 37 lakes they used this method:

1) they took a sample of water from 0.1 to 0.25 m below the surface.  Using a thermos bottle.  This would minimize change of the gas composition of the water with a change of temperature.  The bottle was not sealed, but left out for a while in the air there at the lake (it was "equilibrated with ambient air").  If you were looking for issues you might or might not like this.

2) a sample of air 1m above the lake was taken.

3) they got a gas chromatograph to measure the CO2 in the air above the water sample, as well as in the air from above the lake.  They might have taken the readings right there at the sampling point, or not its not clear. They may have also sealed bottles up and taken them to the lab.  It sort of sounds like a point of sample measurement.

If the air above the water samples had more CO2 than the air above the lake, they called the water supersaturated as the water was emitting CO2.

This method does its best to simplify the question of whether fresh water bodies are saturated with CO2 and emitting it or if they might be absorbing it.  By not outgassing the CO2 in the water and trying to get an absolute content of CO2, they are able to get around the various organisms and minerals in the water and pH which would vary the amount of CO2 the lakes can hold.  they are just focusing on whether the water is giving off CO2.


A doubt in biotech question Which type of gene does not occur naturally in living organisms?

Bt gene
Endogenous cytoplasmic defense gene

The answer is 2.

I can't find out what this gene is! Does it mean the gene for methylation and restriction enzyme synthesis or some such thing? Does it even exist?

P.s. I am just a student and do not have in-depth knowledge of biotech.

Endogenous just means that it is naturally occurring in the organism:

http://www.dictionary.com/browse/endogenous

endogenous cytoplasmic defense gene is a general description of a gene that is cytoplasmic and whose function is defending the organism. There isn't THE Endogenous cytoplasmic defense gene. There are many endogenous cytoplasmic defense genes. Note that it is the protein coded in the gene that is cytoplasmic, not the gene itself. It should say 'gene for endogenous cytoplasmic defense protein'.


What is a good source that will help me classify protists? I am a 15 year old that enjoys looking at the micro world. The only issue that I have is that I can't find a good online source that will help me classify the name of the micro organism that I'm looking at. Does anyone know a place that will help me do this? Thanks in advance.

While not comprehensive, the Portal to Protistology has many resources for exploring the diversity of protozoa. I especially recommend their videos that are really fascinating, focus on distinguishing features of different protists, and may be helpful for identification to some degree. But given your interest you should just explore all the pages on the site, check out the books they recommend (e.g. the Illustrated Guide to Protozoa), and see what is useful for you!


Why does the protection afforded by some vaccines last longer than for others? After reading an answer to the question of How Do White Blood Cells Learn? Or Do They?, I came to wonder something. Specifically,

  The effect of this is that every new B and T cell that your bone marrow makes will recognize a unique, random protein sequence, and you will have billions of these cells floating around in your blood circulation at any given time. These cells however will only float around in circulation for a short period of time before dying and being replaced by other cells with new random sequence receptors.

Assumption: What I gather from this (and the remainder of the answer) is that basically, a vaccine "teaches" the existing white blood cells in your body; eventually, these cells will  be purged, so you will no longer be immune.

However, many vaccines seem to only be once-in-a-lifetime, or at least require a vaccine only once per decade (or less).

Some examples would be the Varicella vaccine, which can last up to 20 years, the Tetanus vaccine, which recommends a booster every 10 years, and the HPV vaccine, which lasts 5-6 years. Durations also vary with Hepatitis, Influenza, Polio, and numerous other common vaccines.

I would assume that, regardless of what a cell has "learned," it is purged with the same likelihood as any other cell; yet, it seems that some "learned" defenses can be retained longer than others. In essence, my question is: Why do some vaccines take longer to "wear off" than others?

(Note: This question is not a duplicate of Why do I need a flu shot every year, while many other vaccinations last years or even a lifetime?; I understand that some pathogens can mutate, so immune cells are of no use against mutated strains since they were not vaccinated against the mutation.)

The first thing I want to make clear is that, the B and T that "will only float around in circulation for a short period of time before dying and being replaced", are not the ones that have already learned to recognise a certain diseases (or vaccine) but rather the naive cells that haven't yet done so. This is also made clear later in the same answer you cited:

  As these injected protein sequences circulate through your blood they
  will eventually bump into a B or T cell that has a receptor that
  recognizes them. When this happens, the B or T cell will now start to
  divide and give rise to long lasting memory cells that express the
  exact same receptor and will therefore recognize the exact same
  protein sequence again in the future. These cells will float around in
  your blood for most of your life and make you 'immune' to the
  recognized pathogen.

In order to understand why some vaccines hold for your whole life, while some need a booster every few years we need to look at the life time or recycling of those memory cells, which stay in your body for much longer than the naive immune cells.

Now we come to the actual answer(s) to your question and there multiple  factors that (can) have an influence on this:

Initial strength of the immune response: Every vaccine (and/or disease) evokes an immune response with a different strength. Generally the stronger the first response is, the more memory cells will be created initially (those actually don't have correspond to the same molecular memory either, they might recognise different aspects of the vaccine/disease) and with more cells available it will take longer until none are left
Natural exposure: memory cells start proliferating when they encounter the molecule (protein/virus/bacteria) which they have 'memorised', if there is an acute infection they will do so a lot in order to produce a lot of antibodies against it. However, even a very small amount of virus/bacteria, that wouldn't actually make you sick, will allow induce them to proliferate and preserve their numbers. Therefore memory cells against a more common or prevalent disease should be more stable in your body, than ones against a very rare one.
There very likely more factors that either I or the whole scientific community don't really know about. Cellular systems and the immune system in generally are rather complicated ...