Evolution of protein and protein efficiency Suppose we have a bacterial protein that performs a function and let's say we can measure the efficiency of the protein. Let's say we have two species, species A and B, both of which have this protein. One of these species, species A, is close to the common ancestor of A and B, in terms of evolutionary distance, while B is farther although for both cases, it took two speciation events to end up with species A and species B.

Let's say for both for species A and species B, we measure the protein efficiency in different environments. The species A protein has the efficiency highest in an environment most similar to its own and the same is true for the species B protein. But let's say we have two situations:

When species A protein has best efficency, it has a lower efficiency compared to species B best efficiency
Species B protein best efficiency is lower than the species A best efficiency

In these two cases, what conclusions can we make in particular about the evolution of the protein itself? Can we show that the protein evolved to a degree to suit the different environment of species B compared to species A?

A few details

  One of these species, species A, is close to the common ancestor of A and B, in terms of evolutionary distance, while B is farther although for both cases, it took two speciation events to end up with species A and species B.

I have two issues here.

I don't understand why this information matter for your question.
There are several metrics of evolutionary distance. In terms of time to common ancestor and therefore, in terms of number of neutral substitutions (it is ok if you don't understand why I talk about neutral substitutions) species A and species B are at exactly the same "evolutionary distance" to any of their common ancestor. However, you may want to talk about evolutionary distance in terms of "By how many standard deviations of a quantitative trait did the mean trait value shifted since the common ancestor (in haldanes unit by definition)", then one species might be more closely related to the ancestor indeed. But in such case, you need to talk about the quantitative trait resulting from protein changes and not directly at the discrete, non-ordinal (nominal) nature of proteins.

And a third general issue I have

As I understand the question, I don't think the question is specific to proteins at all. The question seem rather to relate to "environment specific adaptation in comparative genomics and reaction norms" and would be completely legitimate to look at that at the level of a protein or of a quantitative traits.

To answer your question

You are interested in the measure of fitness as a function of both environment and the protein under consideration. The relationship between the fitness (and other quantitative traits) and the envrionment is referred to as the reaction norm.

Here the graph display the quantitative trait (could be fitness) in the Y axis and environment in the X axis (as it is usually represented).There are two lines, for two different genotypes (the two different proteins in your case).

  Can we show that the protein evolved to a degree to suit the different environment of species B compared to species A?

Well, looking at the graphs it looks like indeed one protein has been under selection in one environment while the other has been under selection under the other environment. Testing this is just a matter of statistics. Basically, to test for this, you run a linear model with the quantiative trait (eventually fitness) as the response variable and the environment, the genotype and their interaction as explainatory variables. If the interaction term is significant (and if the directionality of the interaction is the one you would expect, that is genotypes are more fit in the environment where they live and if each genotype outcompete the other in at least one environment), then the genotypes are locally adapted.

EDIT

  what counts as significant?

You can chose the level of significance that you wish (0.05 for example). If this is unclear, you'll probably want to learn more about stats before.

  can you provide an example of when this method you have described was used the literature to show the evolution of a protein?

If you want example from the literature you can just type Genotype by Environment Interaction on google scholar and will get tons of hits. Here is a paper discussing this methodology specifically and here is a (old) book on the subject. I am not sure why you're still talking about proteins. Most often those studies are done at the level of the gene (or directly on the phenotypic trait). But you can find the gene and get the protein sequence from it or even play around to visualize it with various biophysics softwares.


What does to "evolve" exactly mean? In this article, the author says:

  Evolution isn’t “leading up” to anything, it just drunkenly limps along using the same set of tricks in slightly different orders.

On other occasions, however, the term "evolution" is often deployed as a process that develops gradually, typically from a simple to a more complex form, or from not adapted to more specialized and "fit".

These contrasting interpretations of evolution make me wonder how I should interpret "to evolve" and "evolution" in the context of processes involved in speciation?

A couple of comments, but maybe not an answer; I think misuse is the wrong word - alternative meaning is better. 'Evolve' as a word is much older than the theory of evolution, and has its origin in the Latin evolvere:

  evolve (v.)
      1640s, "to unfold, open out, expand," from Latin evolvere "to unroll, roll out, roll forth, unfold," especially of books; figuratively "to make clear, disclose; to produce, develop,"
  from assimilated form of ex- "out" (see ex-) + volvere "to roll" (see volvox). Meaning "to develop by natural processes to a higher state" is from 1832. Related: Evolved; evolving.

from Online Etymology Dictionary. Implicit in that definition is the laying out of something predetermined, which can relate to going from simpler to more complex.

Also note that Darwin only used the word 'evolve' once in On the Origin of Species (1859), in the final sentence:

  There is grandeur in this view of life, with its several
  powers, having been originally breathed into a few forms or into one;
  and that, whilst this planet has gone cycling on according to the fixed
  law of gravity, from so simple a beginning endless forms most beautiful
  and most wonderful have been, and are being, evolved.

The implication of progress was one reason why Darwin disliked the word 'evolve' and preferred "descent with modification".

The same root was then used as a name to the theory of Evolution, but then in a much more specific sense than the older, general meaning.

If you look back at the etymology above, it is quite clear that biological evolution (The Modern synthesis version) emphazise the connotations 'expand', 'produce' and 'develop', but not the 'unroll' and 'unfold' parts (which both to some extent imply something predetermined).


what is the biggest known functional distance between an enhancer and its target gene (TSS) in cis? since the title seems self explanatory;
It would be nice if anybody could provide a reference. I'm looking for a paper that I belive stated around 1.5 Mb but anything above will be cordialy welcomed.
thanks a lot

I haven't found 1.5 Mb, but 1 Megabase. This is the case for the shh gene in chicken, where the enhancer element is located 1 Mb upstream. The original article can be found here:

"A long-range Shh enhancer regulates expression in the developing
limb and fin and is associated with preaxial polydactyly."

There are two reviews which are also interesting in this context:

When needles look like hay: How to find tissue-specific enhancers in
model organism genomes
Remote control of gene expression.


Is it possible to purify antigens from a vaccine and to separate them from the adjuvant? I need to separate the antigens from several vaccines in order to use them for coating microplates to run an indirect ELISA. I at least need to remove the adjuvant from the vaccines. Is this possible to do and if yes, how do I go about it?

The major component of a vaccine is the adjuvant, and according to Wikipedia the most commonly used adjuvants in human vaccines are aluminium salts.

Here for example is the composition of Recombivax HB, a hepatitis B vaccine produced by Merck Frosst and used in Canada (source of information is a Canadian website)

  RECOMBIVAX HB ® [hepatitis B vaccine (recombinant)] is a non-infectious subunit viral vaccine consisting of surface antigen (HBsAg or Australia antigen) of hepatitis B virus produced in yeast cells. A portion of the hepatitis B virus gene, coding for HBsAg, is cloned into yeast and the vaccine for hepatitis B is produced from cultures of this recombinant yeast strain according to methods developed in the Merck Research Laboratories.
  Two formulations are available:
   •  10 µg/1.0 mL formulation: each 1.0 mL dose contains 10 µg of hepatitis B surface antigen adsorbed onto approximately 0.5 mg of amorphous aluminum hydroxyphosphate;
   •  40 µg/1.0 mL formulation: each 1.0 mL dose contains 40 µg of hepatitis B surface antigen adsorbed onto approximately 0.5 mg of amorphous aluminum hydroxyphosphate;
  Thimerosal (mercury derivative) 1:20,000 (50 µg/mL) has been added only to the preservative-containing formulations. All preparations have been treated with formaldehyde prior to adsorption onto amorphous aluminum hydroxyphosphate. The vaccine is of the adw subtype.

As explained in   Exley, C. et al. (2010) The immunobiology of aluminium adjuvants: how do they really work? Trends in Immunology, 31:103-109:

  The vaccine preparation is primarily micrometer-sized clusters of nano-sized primary particles of the aluminium salt with which the antigen is associated by adsorption and entrapment. The avidity with which the adjuvant associates with the antigen will depend upon multiple factors, including the form of aluminium salt (usually oxyhydroxide or hydroxyphosphate), the physico-chemical properties of the antigen (including its overall charge and molecular weight), the mode of preparation of the antigen-adjuvant complex (for example, ratio of adjuvant to antigen), and the final solution pH. The latter will usually be around neutral (pH 7.0 +/-0.5), and, along with the highly super-saturated state of the aluminium salt, this will ensure that the concentration of soluble aluminium in the vaccine preparation remains below ca 2 mM. Similarly, there will be a variable proportion of antigen, often <1% of the total antigen load, that is not associated directly with the adjuvant, and some of this ‘free’ antigen may also be in a complex with aluminium., what this means is that the protein antigen is not soluble in the vaccine, but rather is adsorbed and/or entrapped in the inorganic particulate material.

What this means is that the protein antigen is not soluble in the vaccine, but rather is adsorbed and/or entrapped in the inorganic particulate material. The antigen itself has of course already been extensively purified before being incorporated into the vaccine, so the task of purifying the antigen from the Recombivax vaccine is one of releasing it from the inorganic adjuvant. The obvious thing to try first would be to isolate the particulate material by centrifugation, and then attempt to release the antigen from this in a soluble form: things to try would be extremes of pH, high salt concentrations, and detergents. SDS-PAGE would be used to monitor how much was released by these treatments.

Now the example that I gave above (Recombivax HB) is fairly straightforward because it contains a single protein antigen. Compare this to Pentacel, given as first vaccination to babies in Canada (same source as before).

  Act-HIB ® Reconstituted with QUADRACEL ®Haemophilus b Conjugate Vaccine (Tetanus Protein – Conjugate) Reconstituted with Component Pertussis Vaccine and Diphtheria and Tetanus Toxoids Adsorbed Combined with Inactivated Poliomyelitis Vaccine.
  Each single dose (approximately 0.5 mL) after reconstitution contains:
   •  purified polyribose ribitol phosphate capsular polysaccharide (PRP) of Haemophilus influenzae type b covalently bound to 20 µg of tetanus protein 10 µg
   •  pertussis toxoid (PT) 20 µg
   •  filamentous haemaglutinin (FHA) 20 µg
   •  fimbrial agglutinogens 2 + 3 (FIM) 5 µg
   •  pertactin (PRN) 3 µg
   •  diphtheria toxoid 15 Lf
   •  tetanus toxoid 5 Lf
   •  poliovirus type 1 (Mahoney) 40 D-antigen units
   •  poliovirus type 2 (MEF1) 8 D-antigen units
   •  poliovirus type 3 (Saukett) 32 D-antigen units
   •  aluminum phosphate 1.5 mg
   •  2-phenoxyethanol (not as a preservative) 0.6% v/v
   •  polysorbate 80 10 ppm (by calculation)
   •  bovine serum ≤50 ng
   •  trace amounts of formaldehyde
   •  trace amounts of polymyxin B and neomycin may be present from the cell growth medium

This vaccine is clearly much more complex, so in this case, once the desired antigen(s) were freed from the adjuvant there would be a need to use standard protein purification techniques to separate the various contaminants.

Finally it's worth pointing out that unless you have access to large amounts of vaccine, you are going to be starting with quite small amounts of antigen (see above) so it will probably be quite a challenging purification.


Why food is still tasty? I'm not a biologist, but it seems that plants with disgusting taste have evolutionary advantage to tasty plants. Same about animals.

There are some species that can not be eaten by man (sharks have poisonous meat). Being eaten by a human — is one of major threats for a shrimp. Does it mean that shrimps are going to become less and less tasty (for a human taste)?

Things are not fundamentally tasty or disgusting. A dung fly loves that taste of dungs while I personally prefer the taste of an apple and my dog prefers the taste of duck fat. A classic example is the gene family TAS2R and the evolution of bitter taste in rodents and primates.

Predator (incl. herbivores) evolves as to like the taste of what he should be eating (Carlsson et al., 2009). Preys (incl. plants) can eventually play out with their taste though, trying to either taste bad to avoid specific predators or taste good to attract specific predators that may disseminate their seeds. I have failed to find evidence that plants can deceive animals at being more tasty than nourishing but you might still want to have a look at Dethier (1980), Sorensen (1983) and Goff and Klee (2006).

One could therefore expect an evolutionary race (red queen) between preys and predators upon how they taste. It would likely be a rather complex race as most species have several predators and several species they prey upon. However, such race on taste would work only if plants can deceive animals which I failed to find evidence for. Arms race for toxic compounds relating to evolution of taste in animals are very much known though (Edger et al., 2015).


Is it true to say that the genome of trees includes or at least "encapsulates" the genome of mushrooms? As a botany amateur, I know that mushrooms (which are of course studied in field of mycology and not botany) are dependent in trees or shrubs (and maybe also bushes) and that there are generally strong symbiotic relations between trees and mushrooms.

If mushrooms are strongly tree dependent and appear per tree species, is it true to say that the genome of trees includes the genome of mushrooms by some mechanism?

No.

Evidence: If you go to the TreeGenes site and examine those tree genomes that have been sequenced you won’t find any fungal chromosome sequences. (And vice versa.)

Reason: Although trees and mushrooms may develop symbiotic relationships they are independently viable (at least the trees), and even two organisms that can only survive in a symbiotic relationship have separate nuclei with separate chromosomes. They are distinguishable, so they are distinguished.


Why do people perceive blood pressure as the force that moves the blood forwards (see details)? For example "Veins contain a lot of valves because the blood pressure inside them is low.". This wouldn't make any sense unless if blood pressure was perceived as the force that drives the blood forwards. But in reality blood pressure is the force exerted by the blood on the inner walls of the blood vessels so can someone explain to me why low blood pressure results in increased likelihood of back flow of blood ?

In the vascular system, pressure is what moves blood forwards, at least in an analogous manner to voltage...just like voltage, pressure itself doesn't move things, but a pressure gradient does. You are correct that the pressure applies in all directions, but the resistance of the blood vessels means that the pressure can only be relieved by flowing in one direction: down the pressure gradient.

Although blood pressure is often medically reported at a single site(i.e., 120/80mmHg), this is only the pressure in the larger vessels. The pressure originates from the heart forcing blood out into the major arteries, and the compliance/elasticity of those vessels keeps a sort of "reservoir" just like a capacitor would in an electrical circuit. The pressure drops over time from systolic to diastolic as that reservoir drains out into the body.

Importantly, and most relevant to your question, blood pressure also drops significantly through space, through the arterioles and capillaries, down to near zero in the venous system:

(from https://legacy.owensboro.kctcs.edu/gcaplan/anat2/notes/APIINotes5%20cardiac_equations.htm)

This pressure drop occurs for the same reason that you get a voltage drop over a resistance in an electrical circuit: the rules of Ohm's law for electricity are analogous to the Poiseuille's Law for fluids.

Sidenote: there are some exceptions to the pressure drop over space in the arterial system because of hydrostatic pressure (i.e., the pressure from gravity, for example see this question, though the better answer is definitely not the accepted one or the one with the most up-votes). However, that hydrostatic pressure difference is offset by gravity in the same direction, so you can effectively ignore it. It is also much less significant once you get to the smallest vessels.

I'm not sure where you got the quote in your example:

  Veins contain a lot of valves because the blood pressure inside them is low.

..but I would say this statement isn't really false, though it could be stated better and the full causation is missing. Veins use valves because a lot of the pressure in the veins is coming from muscle contractions that squeeze the vessels from the outside, not from a pressure wave caused by forced blood volume from the heart. Venous valves ensure that the flow caused by this external pressure travels in one direction.

The Wikipedia page on hemodynamics may be helpful, though I noticed some poor wording in a couple places; any physiology textbook from a major publisher should be a good reference as well.

For a more "ELI5" answer, if the concepts I discussed so far are foreign, try this: In the arteries, blood is moved because the heart fills the big vessels with lots of blood, and the only place it can go is through the vessels into the capillaries. However, because the capillaries are all so thin and skinny, it takes a lot of pressure to push through them, and all the pressure is lost by the time you get to the veins.

So how do we get blood back to the heart? Well, we could try a vacuum, and have the heart "suck" blood back the way it "pushes" out the other side. However, this would collapse the veins. You can suck through a plastic straw because its rigid, but if you make it less rigid, such as by crushing a section, when you suck it will collapse, and sucking harder won't help the situation. Not good!

Okay so it's better to pump, but all the vessels are so small it would be hard to have them each have their own pump. So instead, the veins go through and around various muscles, and when those muscles move, the veins get smushed. Imagine you have a hose full of water, and you jump in the center...oops! Water goes out both ends! Okay, what if you put your hand over one side? Now it only goes out the end you want. That's essentially what a valve does: only lets the flow go one way when things are squeezed. Then the blood stays in the next compartment and over time works its way back to the heart.


Is there any known reason why 6 leg mammals are only found in mutations? Taking a look in internet you can find photos of mutated mammals with 6 legs. Some cows with legs in unnatural positions were shown in website versions of widely known newspapers (you can easily guess here that if the animal gets his additional legs in the back or another unuseful position why a mutation like that wont spread, but the point here it's 2 additional legs in mammals do appear occasionally) . Also there are some dubious photos of sheeps with appparently functional 6 legs, these ones are dubious and hard to confirm if real, some clearly fake but the dubious ones are there and make you wonder. Insects have 6 legs, there are confirmed mutations of mammals with 6 legs, then why did it never appear a mammal species with 6 legs. Is there any known reason why 6 leg mammals are only found in mutations? (how about size and enviroment, is there any reason in those for them not to get 6 legs?)

If stability is the goal, more legs tend to be better. However, having lots of legs also comes with a cost: they take energy to build and use, have extra weight, etc, and they don't really add any speed.

Insects are incredibly successful and likely evolved from many-legged ancestors, losing legs for efficiency but stopping at six. For small creatures with exoskeletons like insects, having fewer than 6 legs means too much loss of stability, because they rely on a tripod of 3 legs while moving the other three.

However, mammals and the vertebrates in general are larger and don't have exoskeletons and can use balancing and moving strategies that insects cannot. Further, they have evolved with four appendages since before they walked on land.

For a 6-legged vertebrate to evolve, there would need to be a selective advantage for having 6 legs versus 4; since vertebrates get along just fine with 4 legs, adding two more isn't likely.

I would also add that just because you can observe mammals with more than 4 legs does not necessarily mean that is a heritable trait. It could instead be caused by environmentally-induced errors in development. I think for the cases you mention this is probably most likely.

Lanham, U. N. (1951). Why do insects have six legs?. Science, 113(2945), 663-663.


How can human infants express chymosin with only a pseudogene at their disposal? I read on the Wikipedia article about Chymosin http://en.m.wikipedia.org/wiki/Chymosin
It stated that chymosin is produced by gastric chief cell in human infants.
But it also stated that human only has a pseudogene for chymosin that does not actually encode the enzyme. On the other hand, another article show that gastric chief cell only secret chymosin in ruminant http://en.m.wikipedia.org/wiki/Gastric_chief_cell
How can infants express chymosin without a functional gene?

TL;DR: Chymosin is similar to pepsin and I couldn't find any evidence of functional/expressed chymosin gene in human genome.

It seems like a common misconception that chymosin is functional in humans. Already in 1940s it has been shown that rennin (aka chymosin) is absent from "gastric juice" in adult humans.

Genetically there is only pseudo-gene for chymosin, as wiki and other sources state. At the same link that leads to chymosin gene page you can find some literature on cloning and structural analysis of chymosin pseudo-gene.

If you use BLAST for finding homologous proteins to chymosin from, say Bos  mutus (aka yak), you can find that in humans closes sequence can be attributed to pepsinogen and similar proteins. Which very much might mean that what is called chymosin in other animals is pepsin in humans, or there is some convergence/divergence which eliminated chymosin in humans. But this is only a speculation.

You can try to scan Google scholar for more sources.

NB link to BLAST search will expire in ~24 hrs.


Can something like McDonalds be considered a life form? "The current definition is that organisms are open systems that maintain homeostasis, are composed of cells, have a life cycle, undergo metabolism, can grow, adapt to their environment, respond to stimuli, reproduce and evolve." (Wikipedia)

Could McDonalds(or any other chain store) be considered a life form according to the current most accepted definition of Life? If not, what am i missing?

It evolves and changes over time; it reproduces by using excess Material to build new stores, it responds to outer stimuli by adapting to them; it grows to a point it is benefical; it starts to function sometime and will eventually stop; it autoregulates it self trying to maintain a stable state and it has a very complex metabolism

Thanks in advance

No. First of all, an "organism" is not automatically a "life form". And it is easy to see that McDonald's does not have an information repository in the form of a genome-like structure, where mutations are quantum-acausal, but still have causal consequences on the bearing reproductive units and they trace an evolutionary path all the way down to the ancestor. In your food stores there is no such a thing. Everything is just engineered and organized by us humans. This is "intelligent design" (although fast food is not really an intelligent thing to do) and has nothing to do with evolution in the biological sense.


What kind of mushroom is this? I picked it this evening beneath an oak, in France, Nantes :

I tried an image search with Google, and it seems I picked a finger of a dead hand :)

What is its name, and is it edible?

The shape, colour and scales on the hat suggest something in the genus Coprinus.

Some species are edible, but it is not recommended to have them with wine.
I would not advise you to eat them without further live identification by someone knowledgeable. Photo identification is not reliable.


Why does the seed of the coconut tree have a liquid in it? What is the purpose of water in the coconut seed?  The reason I ask this is that I was reading about coconut water and all the benefits it has for us Humans.  But why does the tree put a liquid in the seed?  I read a lot more and learned that the liquid becomes a solid and is called endosperm, which is food for the coconut tree.  I'm still not happy with that answer because all seeds are food for the plant they become.  They are also a lot more.

I have come up with a very good explanation for the existence of coconut water and I want see if anyone else has any ideas.  Remember, I am not trying to find out why there is food in the shell.  That's obvious.

It is a transitory state.

During coconut development the "milk" actually starts as a spongy solid a multinucleate endosperm. As the coconut develops it absorbs this tissue. Because of a coconuts hard structure this leaves a cavity since the coconut cannot change shape as the tissue density changes, some fluids including oils are left behind as hte tissue is broken down and reabsorbed. But this fluid will be reabsorbed as the the developing cotyledon fills in the cavity. The fluid is a by product of the cavity but the the cavity is needed due to the unusual development of the coconut.

As a side note most comercial coconut milk is actually squeezed out of the solid endosperm.


Glomerular Filtration Rate In practice, when you have vasoconstriction of the glomerular capillaries and subsequently an increase in blood pressure, glomerular filtration rate increases. However, this seems counterintuitive to Bernoulli's principle.

During vasoconstriction, because the radii of the capillaries are getting smaller, we should expect an increase in flow rate and blood velocity. According to Bernoulli's principle, the outward hydrostatic pressure should drop.

How does this lead to an increase in filtration rate?

The previous answer isn't quite correct, because, well, blood flow is complicated and the body has autoregulatory mechanisms. As Alex mentioned, vasoconstriction doesn't occur in capillaries because they lack a muscle layer. It does occur in the small arterioles before and after the glomerulus (the afferent and efferent arterioles, respectively).

Bernoulli's principle mainly applies to larger arteries and arterioles, and not capillaries. Capillaries are so tiny that the red blood cell is a significant portion of the diameter, so the assumption of no viscosity is no longer valid. See this discussion for an explanation.

To address your question, here's a basic picture of the glomerulus, from Gray's Anatomy.

The afferent arteriole is in red, and the efferent arteriole in blue. The glomerular filtration rate (GFR) depends on the pressure difference between the two, which affects the hydrostatic pressure at the glomerulus. Also, note that vasodilation has the opposite effect of vasoconstriction on GFR.  (For a nice image and explanation, look at Figure 6 here) So:

Constriction of the afferent arteriole decreases the blood flow into the glomerulus and thus the glomerular hydrostatic pressure, which leads to a decrease in GFR.
In contrast, constriction of the efferent arteriole decreases blood flow out of the glomerulus, and this increases the glomerular hydrostatic pressure and leads to an increase in GFR.

Both the afferent and efferent arterioles are regulated through hormones (and drugs that inhibit the hormones). Prostaglandins dilate the afferent arterioles, and NSAIDs inhibit this action. Angiotensin II preferentially constricts the efferent arteriole, and this action is restricted by an ACE inhibitor. (Source: First Aid for the USMLE Step 1)


Sources for common laboratory Saccharomyces strains? I'm used to working with bacteria - some of the more common laboratory strains sometimes come with an order from some vendors.  What's the most convenient source to order common straings of Saccharomyces for lab work?

ATCC is the place I would go to, just like purchasing cell lines or bacterial lines. The reference ATCC catalog numbers are also listed with each of the common strains you have linked. Depending on the purpose, you could just go to your local grocery store for baker's yeast.


Detailed mechanism of the cause of diabetes mellitus type 1? I have read in some texts that diabetes mellitus type 1 is caused by degeneration of beta cells due to our body's own immune reaction.Is it true? Can you explain further how are such types of immune reactions are induced? And are there any other causative factors known?

Diabetes mellitus is divided into four  type 1, type 2, gestational diabetes, and specific type of diabetes. Type 1 diabetes is commonly called as Juvenile diabetes or Brittle diabetes.
It is also called as "Insulin-dependent diabetes mellitus (IDDM)". For our bad-luck the causes of Type 1 diabetes remains obscure, and scientists believes its mostly related to genetics and other environmental factors like mutations or virus attacks. I found some articles that may help.

  But it
  is believed that genetic and environmental factors (possibly viruses)
  may be involved. The aetiology ('cause') of type 1 diabetes is
  unknown, but a good deal is known about its pathogenesis (the way in
  which it develops). As with other complex diseases, the outcome is
  determined by the interplay of multiple genes and (most likely)
  multiple environmental determinants, together with an element of
  happenstance. The risk of developing diabetes is strongly influenced
  by genes affecting immune function, particularly the HLA system,
  but other factors are involved. The best evidence for this comes from
  the study of identical twins: if one twin develops diabetes in
  childhood, the other (who has identical genes) has no more than a one
  in three chance of developing the disease. Prospective studies in
  human populations reveal that circulating auto antibodies directed
  against the islets typically appear in the first 5 years of life, and
  may be present for many years (sometimes 20 years or more) before the
  disease develops. A similar latent period is seen with coeliac
  disease, and implies that some sort of regulatory balance has been
  achieved within the immune system, and subsequently lost. This opens
  the door to the possibility of 're-education' of the immune system by
  various forms of immune intervention.
  Reference

  The pathogenesis of Diabetes mellitus type 1 shows a strong tendency towards genetic related factors,

  Reference


Enzyme Inhibitors: Using in vivo in yeast I find listed on the Sigma-Aldrich site a large list of enzymes & corresponding inhibitors. e.g. For the enzyme squalene synthase the inhibitor listed is "Zaragozic acid A trisodium salt"

Would this mean that if I added the right amount of this chemical to, say, a Yeast cell culture I might expect to get reduced activity of Squalene Synthase which is native to yeast and catalyses the transformation of FPP to Squalenes.

Would this even be a reasonable thing to try if I had a goal to block Squalene synthase? Or am I interpreting how these inhibitors ought to be used incorrectly? Can they be used with in vivo cultures at all?

This is usually the way this kind of inhibitors are used. There needs to be a way that they come into the cells (if they stay in solution and cannot reach their target they will be useless), but then they inhibit their targets.

What usually needs to be done is to determine which concentrations are needed in the cell culture (or the medium) to be effective for the inhibition but not to harm the cells. Therefore I usually use different concentrations of the inhibitor in culture and then measure the outcome.

To find the right concentrations, see if there are some recommendations from the manufacturers. Otherwise you will probably have to dig through Pubmed to find some starting point.


What is the genome size of Saffron (Crocus sativus)? I searched the web but cannot find an answer for my question. Has the genome size of Crocus sativus been determined?

Neither NCBI nor Ensembl have a genome project listed for any crocus species, although individual ethidium bromide stained nuclei have been analyzed by flow cytometry, revealing approximately 11.4 pg of DNA per nucleus (warning, pay wall).

C. sativus is triploid, giving it a C-value of 3.8 pg which works out to a haploid genetic content of about 3.45 Gbp.

(full credit to canadianer for finding the Brandizzi paper)


How to do whole genome sequence alignment in R or Ruby/C++, any good language? I need to perform tuberculosis mutation analysis. First step I need to do is to align sequences in fasta format against one reference file. i tried CLC genomics workstation --- it hangs on 60 000 lines of fasta reference file for entire day. Please advise what technology and tutorial to use to do that task.

I think you incorrectly identified what type of analysis you want.  You mention that you have numerous sequences in a fasta file (you mention at least 60,000) that need to be aligned to a single genome.  So your not doing a pairwise alignment, your aligning DNA sequences to a reference genome.  The fastest known algorithm for this is burrow-wheeler transformation mappings which can be accomplished with tools such as bowtie, bowtie2, BWA, etc...

I'm assuming your experimental design is something like this: You have sequencing data from a number of tissue samples with half or some number of samples being a disease state, the other being normal.  So you want to create alignment files for each sample, and than determine where these alignments differ.

After alignment, you will need to create a variant file (VCF) which can be accomplished using samtools or GATK.  The VCF file will give you all bp locations with alternative alleles from your reference genome.  Which seems to be what your looking for.

Citations that could be useful:

Langmead B, Salzberg S. Fast gapped-read alignment with Bowtie 2. Nature Methods. 2012, 9:357-359.

Bioinformatics. 2011 Nov 1;27(21):2987-93. doi: 10.1093/bioinformatics/btr509

Li H. and Durbin R. (2009) Fast and accurate short read alignment with Burrows-Wheeler Transform. Bioinformatics, 25:1754-60. [PMID: 19451168]

Li H., Handsaker B., Wysoker A., Fennell T., Ruan J., Homer N., Marth G., Abecasis G., Durbin R. and 1000 Genome Project Data Processing Subgroup (2009) The Sequence alignment/map (SAM) format and SAMtools. Bioinformatics, 25, 2078-9. [PMID: 19505943]

https://www.broadinstitute.org/gatk/about/cited-by

The last url contains 145 publications that used GATK to look at population-scale variant differences.  These publications could be very useful to see how other papers have accomplished variant discovery for the use for scientific inference.

For User137 - since I can't comment on this board yet; you want to use a program called muscle.  There is an MS-DOS version and it can align short sequences extremely fast.


Why doesn't muscle strength depend on its length? In case of tug of war the more people participate the more strength they represent. And in case of muscles - the longer it is, the greater the number of myosin heads bind to actin when muscles contract. So why doesn't length matter?
UPDATE:
Since I've found multiple answers that compare muscles to ropes, let me comment on why those explanations don't work for me. Ropes don't have "muscle" strength, they have tensile strength. So this analogy can only compare tensile muscle strength to tensile rope strength.
In the end I'm pretty sure I'll find out that tensile strength constraints the muscle strength. And that's probably going to be the reason why muscle strength doesn't grow with length - something does not allow it, otherwise it would get damaged.
But I'd like find out what exactly prevents further contraction. Is it mechanical receptors on the muscle cell which block deploarization? Mechanical receptors in tendons which send nervous signals (but then - do tendons get thicker in proportion with the muscle)? Something else?

It's simply that the fibers are arranged end-to-end. If you simplify this down and imagine a single muscle fiber you have actin and myosin like this:
ligament-|actin-myosin-actin-myosin-actin-myosin

If you think of this as a strand of cotton pulling on a weight (ligament). Each group only pulls along the length, so the strength is not multiplied, but rather related to the strength of the individual fibre.
In reality muscles are stacked into bundles, which are much stronger as all the fibers can contract pulling with the strength of the multiple ends. Like this:
         |actin-myosin
         |actin-myosin
ligament-|actin-myosin
         |actin-myosin
         |actin-myosin

This is like the multiple strands of cotton making up a rope, the strength comes from having lots of them distributing the load.
This is something called physiological cross-sectional area, which describes the strength of a muscle by estimating the cross-section of the muscle across its thickest part.


Do biologists use the word "solubilize" to mean "dissolve"? I work with biologists who often use the word "solubilize" to mean "dissolve".
Is this correct usage? I keep correcting them (I'm not a biologist, but I help with writing), and we've argued about it. Not all are native English speakers, so I've been attributing it to that. But maybe they're right. I want to know.
The context here is pharmacology - taking drugs in powder form and dissolving them in a vehicle for dosing lab animals.
I thought "solubilize" means to make something more soluble by adding (for example) soap. (for example: https://www.thefreedictionary.com/solubilisation ).
But they use "solubilize" to mean "dissolve". That usage doesn't seem to be standard English, but maybe it's normal usage as a term of art in pharmacology.
Is it?
For scientific writing in pharmacology, what is the standard usage? When we mean (standard English) "dissolve", which word should we be using, in order to be clearly understood and conform with standard professional terminology?

Added: Some of the commenters seem to misunderstand what I'm trying to ask, so I'll try to clarify.
I can read dictionaries as well as you can, and Google is my friend, too; I'm not asking what the standard dictionary definitions are (I already know).
I'm asking about how working biologists, English-speakers, use these words.
Do practicing biologists/pharmacologists use these terms differently than the standard English definitions? Are these "terms of art" in those fields, with a different definition? Or not?
Some of my colleagues insist that, in their field of biology/pharmacology, the word "solubilize" is used to mean what the dictionary says "dissolve" means. Are they correct, or are they mistaken (presumably because they're not native English speakers)?
I'm not a biologist and so don't know from personal experience. The people I work with are biologists but not native English speakers, so I'm not convinced they know either.
Thus, I'm asking here.

I've been asked for a sample sentence re how it's used. I don't see how that affects the answer, but here:
"Diphtheria toxin (List Biological Laboratories, Cat #150) was solubilized in sterile water at 2 mg/mL, aliquoted, and frozen at -20 C."
Is this correct usage or would "dissolved in sterile water" be better?

I think I found an answer at Science Direct where multiple definitions are provided, among one from Thomson (2012):

Solubilization is the action of certain chemical reagents on organic materials (such as animal or plant tissue) that effects a structural breakdown (or digestion) into a liquid form that can then be directly dissolved [...]

and from Lau (2011):

Solubilization is the increase in solubility of a poorly water–soluble substance with surface-active agents. The mechanism involves entrapment (adsorbed or dissolved) of molecules in micelles and the tendency of surfactants to form colloidal aggregations at critical micelle concentration levels.

From these definitions I understand that solubilization is a process to make something dissolvable. The process of dissolving thus happens after the solubilization (definition #1) or during the process of solubilization process (definition #2). Thus, solubilization and dissolving are separate processes (definition #1) or dissolving is considered a part of the process of solubilization (definition #2).
So admittedly, at this stage I am unsure to what exactly the two terms mean exactly, but they are certainly not interchangeable terms.
And regarding your comment

...that it's not unusual for experienced biologists themselves to be unsure which is the proper term here. Even native English speakers

I totally second Bryan's response

Language is messy, scientific terminology included...

This is because terminology tends to stick after having been adopted widely, even if it proves to be incorrect. Consider for instance the fact that current always flows from + to - in schematics, but that electrons definiely choose to go the other way around. Scientific terminology is messy indeed.
References
- Lau, Preformulation Studies. In: Handbook of Modern Pharmaceutical Analysis: 173-233
- Thomson, Handbook of Radioactivity Analysis (3rd ed.) 2012: 575-623


Why is a slow worm not considered a snake? Slow worms are considered lizards as opposed to snakes, both are reptiles. Now I get that there are traits that distinguish them (eye lids, ears ...). But snake species themselves vary already quite a lot.

The Wikipedia article on snakes states:

  Based on comparative anatomy, there is consensus that snakes descended from lizards.

But how comes slow worms are considered lizards despite the loss of their limbs during evolution, whereas the same evidently has happened to snakes?

What's the defining factor here? The time frame when it happened, that it happened independently (like the evolution of, say, an eye)?

Note: I couldn't find any detailed descriptions about the alleged evolution of slow worms, whereas for snakes it is easy to find material.

You are correct that the reason is similar to that of convergent evolution of the eye.

Both snakes and legless lizards are lizards (Squamata) that have lost their legs. However they have done so entirely separately much as octopus and human eyes have evolved entirely separately. An easier analogy is between whales and sea cows. Both are legless mammals but as they have evolved separately the must be given separate names.

Unfortunately it seems that the exact position of the snakes in the tree is unknown which makes this explanation less clear.

http://tolweb.org/Squamata/14933

However, the legless lizards (subfamily Anguinae) are within the family Anguidae, most of which have legs. This family is within the Anguimorpha, which includes even more species with legs. Just one small tip of the tree, with around 20 species is legless. On the other side of the tree, separated by many millions of years is the snakes (Serpentes).

A related question is why are snakes given their own name while legless lizards are just considered lizards without legs. This is partially due to the fact that there are so few species of legless lizard while there are thousands of species of snake. It is also probably due to cultural history. As snakes are dangerous to humans and prevalent in most inhabited areas of the world words for snakes are much older than the study of taxonomy. A western example is the snake in the garden of Eden. It is also important in Hinduism
and many other cultures/religions.


Perception of artificial light - flickering I noticed something strange a couple of years ago. I was walking down the street at night, when it struck me that the street lights were flickering. But, when I turned to take a direct look at the light source it did not flicker any more. In other words, when the light is not the main focus of your eye, it can flicker.

From then on, I started to focus on these flickerings and they are everywhere. Street lights, lights in a house, but also computer monitors or even projections on a screen. Again, the flickering only happens when you do not look directly at the source.

Does anyone have an explanation for that? Is it the brain's fault, or the eye's?

It's difficult to give an exact answer without actually observing the light and performing measurements. I have a theory, though.

Your peripheral vision is hyper-sensitive to changes in light - an evolutionary trait that provided quicker reactions to predators sneaking up on you. As such, even the tiniest fluctuations in light can be registered with your peripheral vision; much more so than your primary field of vision. In this case, it may well have been that the light was flickering very subtly, or at a very high frequency, which your primary field of vision could not pick up. When your peripheral vision was in play, it immediately spotted the flicker.

This is reliant on a principle called the flicker fusion threshold, which essentially states that there is a threshold of various light properties (including flicker frequency, colour, intensity, etc.) at which an eye begins to distinguish a steady light from a flickering one. Research has demonstrated that species who have high rod density are good at picking up flickering, whereas species with low rod densities have a much poorer threshold. Cone density doesn't seem to factor in very much, since flickering is primarily a change of intensity rather than hue.

This transfers into the human eye, since we have a high rod density (and low cone density) at the edges of our retinas, i.e. in our peripheral vision. If you had the eyes of another species (as creepy as that would be) with a high rod density, you may well have been able to detect the flicker quite easily with your primary field of vision.

To directly answer your question - yes, I believe this is primarily the "fault" of the eye, rather than the brain. The brain has a role in identifying the flicker at a subconscious level, in terms of fight or flight response, but the eye is responsible for providing the elevated sensitivity at the peripheral.


Any nerves/fibers in foot similar to ulnar nerve in elbow? I just noticed that when I gently run my fingers along the top of my right foot, I get the same exact "funnybone" sensation in my toes that I get when I hit the ulnar nerve in my elbow.

So I ask: are there similar nerves/fibrous structures running along the top of your foot as whatever is going on in your elbow with the ulnar nerve?

Not medical advice; just curious about the anatomy here.

Why would peripheral anatomy determine subjective sensation? In the end, the cerebral cortex determines the sensation associated with peripheral input. Rewired hamsters can have visual sensations in their auditory cortex (Frost et al., 2000) and visual sensations through tactile stimulation have been reported in man (Ortiz et al., 2011).

The sensations you describe are related to tactile stimulation of peripheral nerves. Peripheral nerves are pretty homogenous, and typically carry a bunch of afferent nerve fibers up to the somatosensory cortex.

References
- Frost et al., PNAS (2000); 97(20): 11068–73
- Ortiz et al., PLOSone (2011)


Question to the color scientists I have a question.
if you look at these two spectral diagrams (SPDs) from two different televisions that is calibrated to the same white point (D65) 6500K with a spectrometer.
The problem is that white still looks different to the eye here.
why does white look different is my question.

Television1
(pictures from avsforum)

Television2

A logical explanation would be great as i trying to figure out whats causing it.
is it the spectral power differences that causing it or is it the different distribution of the GREEN and RED with its more narrow peaks on television1 that causes it?
what i can see and what i understand is that Television1s spectral power will produce a more natural light as its more close to the warm light from an incandescent bulb.
Television2 reminds more of an typical LED lamp that we all know have a more harsh and poor light.

After more reading and information its quite simple.
our eyes picks up the energy from the primary colors.
if a television has higher BLUE energy than RED and GREEN that picture will have a blueish cold look to it even if its calibrated to D65

the SPD from television nr1 has higher energy for GREEN and RED and so whites on this television will look more warm and less blue.

how distinct and separate the cones are can also matter here.
television nr1 has no clear separation between GREEN and RED while television nr1 has.


Two brown-haired people have two children, P and Q. P has blond hair. Q has brown hair. What is the probability that Q is heterozygous? Two brown-haired people have two children, P and Q. P has blond hair. We therefore believe that each parent is heterozygous and that blond hair is a recessive trait.
Q has brown hair. What is the probability that Q is heterozygous?

My answer:  2/3.  There are four possibilities Bb, bB, BB,and bb. Before observing the color of Q's hair, we assign equal chance to each.  We eliminate bb as a possibility.  The chance that it is bB or Bb and not BB is 2/3.

A Biology PhD disagrees with me and says that the probability is 1/2. Who is right?

Assumptions: Blonde hair is Homozygous Recessive and that the traits are strictly Mendelian.

The parental generation must be both heterozygotes as at least one child is Blonde (bb). So your cross is Bb x Bb.

Your square is going to look like this:

           _B_            _b_

_B_         BB           Bb

_b_         bB           bb

So of the question is:

  What is the probability that Q is heterozygous?

The PhD is INCORRECT. They probably just made a simple Punnet Square in their head and forgot the caveat that you have to exclude "bb" because Q is not Blonde. The possible allele combinations for non-Blonde offspring from a Heterozygotic cross are only BB, bB, Bb.

Therefor the probability that Q is Heterozygous is indeed 2/3 (bB, Bb).

It's not uncommon for PhD students - who are often deep into their own research - to gloss over details and possibly give incorrect answers because the information hasn't been relevant to them for years (most traits aren't Mendelian, strictly recessive or dominant, and rarely involve a single allele), so give them some slack unless they were being a jerk about it. =)


In a tumor, why hypoxic regions have access to glucose? The Warburg effect is ubiquitous in cancer. It consists of the upregulation of glucose uptake, glycolysis, and subsequent lactate secretion, sometimes by over 200 times, in cancer cells as compared to normal cells. A common explanation for this phenomenon is that tumor cells can be oxygen deprived, because they are far away from the diffusive range of oxygen in the blood supply. But if that's the case, then how are they close enough to blood supply to have access to enough glucose? How can glucose diffuse to places where oxygen cannot, even if oxygen is a much smaller molecule?

I think this is a difficult question for which the answer is not clear --- to my knowledge there is little data on metabolism in solid tumors, and no clear consensus in the scientific community. So I'm not going to attempt to give a definitive answer, but here's at least a few thoughts / opinions.

Why transformed cells engage in aerobic glycolysis, or the "Warburg effect", is a question people have been trying to answer for nearly a hundred years now. There are dozens of hypotheses, but none of them is broadly accepted. One popular hypothesis laid out by Gilles & Gatenby says that transformed cells from solid tumors are glycolytic because they have been selected for anaerobic metabolism in a hypoxic environment, and this selection is somehow irreversible, so that the cells stay glycolytic even after being extracted from the tumor and cultured in aerobic conditions. I think this hypothesis is the origin of the idea of hypoxic and yet glycolytic tumors.

In a way the Gilles & Gatenby hypothesis is a clever idea --- it rests on the well-accepted fact that most cells become glycolytic in hypoxia, and rhymes with the concept of selection for survival in tumors. But the problem with the argument (as you have realized) is that the tumor environment would have to be low in oxygen and at the same time high in glucose. I agree with you that it is unlikely that such an environment could arise due to lack of blood supply, since oxygen diffuses more easily through tissues (and cells) than glucose does. Moreover, considering the high demand for glucose by glycolytic cells, glucose should become limiting long before oxygen runs out. So one can argue that poorly vascularized tumors should be mainly oxidative, not glycolytic!

To my knowledge, there is no data demonstrating existence of (regions of) solid tumors with low oxygen and high glucose. There is of course ample evidence that many solid tumors consume large amounts of glucose, and also many studies showing hypoxic regions in tumors. But most likely these are different types of tumors, or different regions. In an environment with neither oxygen nor glucose, cells will simply die --- which is exactly what happens in the necrotic cores of larger solid tumors.

The best source of further information is probably the tumor physiology literature. This review is a good starting point.

Finally, another issue with Gilles & Gatenby's hypothesis is that aerobic glycolysis can easily be demonstrated in cells that have never been in a tumor. For example, in vitro transformation can increase glycolysis, and normal lymphocytes induce rapid glycolysis when activated by receptor stimulation. So there is no need to assume that glycolytic tumors are hypoxic.


How interrelated are computational biology and biophysics? I am considering applying to Ph.D. programs, and am not sure what direction to take. I'm hoping you all can help me out.

I have a background in both biology (molecular focus) and physics (condensed matter and math, heavy on theory). Several years industry experience working in labs doing molecular biology and genetics research.

My primary interest is in mathematical modeling of biological systems, and taking this knowledge to then engineer function. Essentially, what I view as a combination of biophysics, systems biology, and synthetic biology.

Here is the dilemma. It is important for me, should I pursue a Ph.D., to have a solid foundation and training in fundamental principles in physics and math, because I want to be able to derive new theories, models, and methods when needed. This leads me to think biophysics or applied math is the "right" area to do my Ph.D in. But biophysics is very broad and systems biology is only a small part. It is also removed from applications in bioengineering.

I know computational and systems biology intermingles biophysics, applied math, genetics, computer science, and various other fields. It also seems like the type of research I am interested in is typically done in computational and systems biology groups. But I'd like to know if computational biologists, aside from doing simulations, also commonly do work in deriving new models/theories in biophysics. Or do they generally apply this knowledge to build simulations and understand data sets (i.e. removed from fundamental biophysics research)? I don't want to be a programmer -- I want to be a theorist who uses computational tools (and only programs when it's needed to simulate something) to solve problems that can't be solved analytically.

Is computational and systems biology an appropriate "umbrella term" for what I'd like to do? Or would I be better suited in a physics Ph.D. program, and attempt to bridge that training towards systems biology research?

Also, how difficult is it to change to a related field if the opportunity arises? Can computational biologists, who are also interested in engineering work, build a model of a system and then work with others to help engineer it?

My overall concern is pigeonholing myself into a field that I don't want to spend decades working in. I want to maintain flexibility along the range of biophysics to bioengineering, and work on problems when the need arises. Also, what field do my research interests actually fall under? I find it often depends on the university and specific department, so it's a hard question for me to answer myself....

Thanks in advance for any input.

Computational Biology is just the application of computers to solve problems in biology. It may mean using machine learning to identify regulatory regions in DNA or it may be solving a complex system of differential equations to model chemical reactions in some metabolic pathway. Whether a background in physics, chemistry, biology, math, or computer science is more central depends on the exact problem you want to work on,  and in fact which aspect of the problem you want to work on.

  Also, what field do my research interests actually fall under? I find
  it often depends on the university and specific department,

Bingo! Your interests are clearly cross-disciplinary, so for any given research question, different researchers in different fields will all be working on different aspects of the problem. Academic disciplines don't get to declare monopolies on research problems!

You Ph.D. is going to require you to spend 4-6 years working on a VERY specific problem. It would be wonderful if you could figure out exactly which research problem you wanted to dedicate the next 6 years to, and then choose the Ph.D. program based on their research program on that problem. This is rare though. More typically Ph.D. students have to spend a year or two doing rotations and talking to potential mentors before picking a research problem. In that case you are going to have to decide which academic discipline attracts you more, and then find a department in that discipline that seems to have a lot of collaborations with the other disciplines that attract you. See Buridan's Ass;


Did the old world have relatives of plants which were brought after the discovery of Americas? When the Americas were discovered many plants were brought back to Europe. For example: potato, tomato, strawberries, chilies etc. At the same time many animals were brought to the Americas including: horses, cattle, sheep, and camels. It seems from the records that there were relatives of these animals in the Americas — for example llamas are in the same family (Camelidae) as camels. I wonder if there were relatives of these vegetables from the Americas already present in Europe or anywhere else in the old world.

Three of your examples: potato, tomato, and chilies, are from the genus Solanum. Along with the rest of the Solanaceae family, they are most diverse in the Americas but some species are found worldwide.

Species that would be found originally in the 'old world' from the Solanum genus and Solanaceae family include the black nightshade, bittersweet nightshade, and deadly nightshade. There is also at least one cultivated plant variously known as eggplant, aubergine, or brinjal (Solanum melongena) that is thought to have been domesticated in Asia.

The strawberry genus, Fragaria, also has species world-wide.

Of course, because all life on Earth is related, the answer to the general question "are there relatives of X found in some place" will always be "yes" as long as there is life there, it's only a matter of the extent of relation.


Is there a term for the opposite of intergenic? I am looking for a term that describes DNA regions that overlap genes, i.e., non-intergenic DNA regions.
For example, say I am writing a paper about DNA-binding sites (i.e., DNA sequences that proteins bind to), but my paper focuses exclusively on DNA-binding sites that happen to overlap genes. What would my title be? "Non-intergenic DNA-binding sites are [...]" is one option, but I wonder whether a more appropriate term exists.
If I understand correctly, "Gene-overlapping" seems to be used for referring to genes that overlap other genes (https://en.wikipedia.org/wiki/Overlapping_gene).
Also, Google says that "genic" means "relating to genes".
Is any of my ideas appropriate? Or maybe another term?

To clarify what I mean by intergenic and non-intergenic, here is the figure from https://en.wikipedia.org/wiki/Intergenic_region. I added an example for a non-intergenic DNA region.

Explicitly, an intergenic DNA region is a DNA region that doesn't share any base with any gene. A non-intergenic DNA region is a DNA region that shares at least one base with a gene.

It seems to me that "genic" is a perfectly good word.
This paper uses "genic" directly as a contrast to "intergenic", so that seems like a reasonable precedent:

‘Noncoding DNA’ can be found both surrounding genes, and within genes (see schematic Figure 1). We will call the first type ‘intergenic’, and the second type ‘genic’, a ‘gene’ referring here to a transcribed DNA sequence.


What is meant by clones of B-cells? I was reading Cellular and Molecular Immunology
By Abul K. Abbas, Andrew H. H. Lichtman, Shiv Pillai and stumbled upon the following excerpt $-$

  In every individual there are millions of different clones of B-cells,each producing antibody molecules with the same antigen binding site and different in this site from the antibodies produced by other clones.

What are these clones of B-cells, one producing monoclonal antibodies and the other polyclonal antibodies?

When you read further you'll get it. Basically, when the antibody expressed on a B-cell recognizes an antigen, then the B-cell divides and expands its population to produce more antibodies (through plasma cells). This process is called clonal expansion.


Atrial contraction in complete SA block In a complete SA block when there's block of impulse from SA node to Atrial syncitium, The ventricles start pumping at AV nodal rhythm but how do the atria then contract?

It depends.

It's likely that another point starts setting the pace instead of the SA node. More infos about cardiac pacing on Wikipedia

Or maybe different points try to set the pace contemporary, without generating a valid contraction but only electrical activity (such as in atrial fibrillation/AF, a very common disease mostly in elders).

An electrocardiogram could answer the question for the specific patient. If there is completely no atrial activity you'll find no P waves (no atrial activity) or baseline continuous little waves (in case of AF because of the irregular atrial activity) and probably bradycardia (because the pacer in the AV node is slower than the SA node).


The gender of offspring of Twins? Given identical twin males, Michael and Douglas, Douglas and his wife have four children, all of whom are girls.  Michael and his wife have only one child, a boy, and are expecting another. What are the chances it will be another boy? If Michael and his wife have more children, what are the chances they will all be boys? Is there any support/evidence for, or a study about, one twin of an identical pair will have children all of the same gender and the other twin will have children all of the same (or opposite) gender?

Note: This is based on literature searches I've done a while ago out of general curiosity. I'm in no way an expert on human reproduction.

If I understand you correctly you are basically asking if there are any evidence for sex biases in offspring between families, that has a heritable genetic basis. This has been an active research topic for a long time and there are a number of proposed mechanisms for how this can be achieved. Historical data sometimes shows deviations in sex ratios over time, e.g. in 20th centrury Europe after WWI and WWII (see data in Gellatly, 2009). There are also other reported/hypothesized deviations in sex ratio e.g. trends in sex ratio due to paternal age (e.g. Jacobsen et al, 1999), sex biases of offspring due to earlier insemination in the menstrual cycle, and the child rank. However, from what I've seen, the evidence hasn't been conclusive and different studies point in different directions.

As Irving et al (1999) point out, possible mechanisms for sex ratio biases can be:

deviations in X/Y-ratio of sperm
selection of sperm within the female reproductive tract
biases in implantation success and/or survival for embryos of different sex

Most evidence seems to point against explanation one, see tests in e.g. Irving et al (1999) and Graffelman et al (1999). Graffelman et al (1999) also tests for an effect of male age, but do not find support for this idea.

Another interesting study is Curtsinger et al (1983), which tries to look at vertical population transmission of sex ratio variation in Japan. They conclude that there is a marginally significant effect on the paternal side, which would support the idea that sex biases might run in families.

  An analysis of vertical transmission of sex-ratio modifying factors that excludes effects of birth order in both the parental and offspring generations has detected a marginally significant paternal effect.

However, they also conclude that the genetic variability in sex ratio is very small, if there is one. This study also does not find support for effects of e.g. paternal age or child birth order.

Gellatly (2009) provides a model of how an autocorrelation in sex ratio between generations could be explaned (while still having a stable population-level sex ratio), using an autosomal gene modifying male sex ratio. Note thought that this is a proposed model, and not empirical evidence. However, Gellatly (2009) also use genealogical/pedigree data from North America and Europe to show that there is an heritable component in the human sex ratio (an association between sex ratio in F1 and F2 generations). However, from what I can see the evidence is weak, and the models only explains 0.5% of the variance in the data. The introduction to this paper also has a useful overview of the subject with more references you might want to check out.

All in all, my perception is that there are some evidence that certain sexes can be overrepresented in families, which could potentially mean that the sex ratio in the offspring of a twin brother can contain information on the probablility that his brother will have a son or daughter. However, to me, the evidence is far from conclusive and the estimated effects seem rather weak. So as a null hypothesis, you should definately go for a 50/50 chance of a son/daughter, irrespectively of what the sex ratio of the twin brother is.

As for the general calculation of probabilities of different scenarios, you just use the product of probabilities and sometimes summation of birth orders. For instance (if assuming 50/50 sex ratio), the probability of having three sons is $0.5^3= 12.5\%$ (births: MMM) and the probability of having 2 sons and one daughter is $3*0.5^3= 37.5\%$ (births: FMM, MFM or MMF, i.e. three ways to achieve this scenario out of eight).


Phytomass and photosynthesis I have been introduced to the term "phytomass" and I was wondering if phytomass can be both photosynthetic and non-photosynthetic?

"Biomass is defined as live material, necromass as dead, attached material.
Biomass + necromass form the "standing crop" or phytomass." (from https://link.springer.com/chapter/10.1007%2F978-3-642-68786-0_22)

But even if we were only talking about biomass, there is only a loose correlation between that and photosynthetic activity -  think about single-celled algae, where 'every' cell is photosynthesizing, versus trees, where most cells are non-photosynthesizing, and there may even be times where none are (in trees that loose their foliage in winter).


Fauna in deep great lakes A significant amount of research has gone into the fauna of the deep oceans, but not so much that I can find on the deep great lakes (specifically the North American Great Lakes).  I'm interested in seeing pictures and learning more about the types of fauna in these lakes.  Can anyone provide a reference to get me going?

Contrary to oceans, deep lakes are always isolated from other deep lakes by land. Therefore, one might expect different fauna in every lake, with possibly a lot of endemic species. So it may be hard to study deep lakes in general.

The ancient and deep lake Ohrid, in the former yugoslav republic of Macedonia, has been researched relatively well. Here's a reference which will get you started. Or search "lake ohrid fauna".


What is the difference between the neural tube and the dorsal ventral cord? I was wondering what the difference is between the neural tube and the dorsal ventral cord.
I know that the neural tube forms during embryonic development from the ectoderm layer that folds inwards.
I thought that the neural tube gave rise to the central nervous system, however sometimes I see the following:

  "the central nervous system develops from the hollow dorsal nerve
  cord"
   for example: https://en.wikipedia.org/wiki/Dorsal_nerve_cord

question
What is the difference between the neural tube and the dorsal ventral cord or are they both the same?
(talking about humans)

The terminology can be confusing, and I suspect the question you meant to ask was: what is the difference between the neural tube and dorsal nerve cord?

In vertebrates, the neural tube and the dorsal nerve cord are two names for the same structure. It develops into the brain and spinal cord.

  Neurulation occurs during the early embryogenesis of chordates, and
  it results in the formation of the neural tube, a dorsal hollow nerve
  cord that constitutes the rudiment of the entire adult central nervous
  system.

Source: Colas J-F and Schoenwolf GC. Towards a cellular and molecular understanding of neurulation. Developmental Dynamics. 2001. vol 221(2): 117–145.

This differs from invertebrates, some of which have a ventral nerve cord that does not invaginate and form a neural tube. As the name suggests, in contrast to vertebrates the nerve cord in these species is located ventrally.

In summary:
Dorsal nerve cord = neural tube
Ventral nerve cord ≠ neural tube


Doxorubicin's intercalant and topoisomerase inhibition in leukemia? I am thinking the role of doxorubicin's pathways in cancers such as leukemia and lymphoma:

topoisomerase inhibitor and inhibit DNA activity
intercalant - intercalant DNA bases and inhibit DNA activity

I am interested in which of these mechanisms are most relevant in leukemia and lymphoma.

How does doxorubicin work in leukemia and lymphoma?

Doxorubicin is part of chemotherapy drugs. Most of them are targeting proliferation of cells, e.g. by blocking cell division or DNA replication.

Intercalants and topoisomerase inhibitors are powerful in interfering with DNA replication (not DNA activity). Other chemo drugs might inhibit proper operation of cell division machinery, such as through interfering with cytoskeleton functions.


What is a CAG::ChR2 rat? I am reading the paper: Pyramidal Cell-Interneuron Interactions Underlie Hippocampal Ripple Oscillations.
The authors use CAG::ChR2 rats (for example in Figure 2) and I don't know what it means.
I understand for example that in PV::ChR2 mice, parvalbumin neurons will be activated by light.
I am also familiar with types of other interneurons (Ivy, Martinotti, OLM, LTS, Bistratified, Mopp, VIP, Somatostatin...)
but I have never encountered CAG cells.

Is CAG represent a type of neuron? or, maybe it represents something else?

Thanks!

CAG is a synthetic, ubiquitous promoter which combines elements of the CMV early enhancer, the chicken β-actin gene, and the splice acceptor of rabbit β-globin. According to the researchers who created it:

  The elements which constitute the pABWN vector, the CAG promoter, the weak neo unit, and the BPV fragment have only low specificity to cell types or species. Therefore, this system can be applied not only to L cells or CHO cells, but to a wide variety of cell lines. The pABWN vector should be very useful for producing large amounts of valuable proteins in mammalian cells, for changing the phenotype of host cells by overexpression of some normal or mutated genes, and for disrupting the function of targeted genes by overproduction of anti-sense RNAs.

In the paper you cite, CAG-ChR2 is used to activate all neurons in the vicinity of the light stimulation, for example in Figure 2Ab, where the panel is labeled "PYR+INT activation."


What is this beetle looking fly creature? I found this fly in my back garden that looks like a beetle with wings and it hovers.

  ]1

  ]2

What is it?

It is of course it is difficult to tell exactly from the quality of the image, but with mandibles of that size relative to the body (approx. 20-25% of total length) it is very likely to be a male Stag Beetle Lucanus cervus, the mandibles will grow much larger. The antenna sticking out from the side of the head just in front of the eye matches your photo (note: in the image below it looks like two on each side, but it is just the shadow in the photo)

Picture from Wikimedia commons https://commons.wikimedia.org/wiki/File:Lucanus_cervus_1922.png

They can be found flying at dusk, and are found in the SE of England from late May to August.

If you are looking for a good insect ID book, I can recommend "A comprehensive guide to Insects of Britain & Ireland" by Paul D. Brock, published in 2014


Definition of the different DNA regions Reading from Oshima et al. (2016):

  We identified 3,868 noncoding mutations including 394 located <5 Kb downstream, 1,762 intergenic, 1,621 intronic, 81 <5 Kb upstream, 7 UTR 3′, 2 UTR 5′, and 1 intragenic variants.

How upstream, downstream and intragenic variants are defined? Shouldn't intragenic variants be classified within intronic variants, and upstream/downstream within intergenic variants?

Edit: By adding the different numbers it seems they are mutual exclusive. While upstream/downstream variants can be defined as intergenic variants that lie close to genes, I haven't found a definition to tell the intragenic variants from the intronic ones.

Edit 2: The only explanation I could think of for intragenic variant is that it is located in a coding region which is not transcribed due to alternative splicing. Can it be possible?

Oshima, Koichi, et al. "Mutational landscape, clonal evolution patterns, and role of RAS mutations in relapsed acute lymphoblastic leukemia." Proceedings of the National Academy of Sciences (2016): 201608420.

We can take a look at the following picture (from wikipedia):

The regions are then:

intergenic: everything outside of the shown gene region
<5 Kb downstream: outside of the transcribed region, but possibly part of the promoter or an enhancer (yellow boxes before coding region).
UTR 5′: in the transcribed region, but not part of the coding region, as shown in the picture (blue box before coding region).
intronic: In the Introns, as shown in the picture (grey boxes)
intragenic: These have to be mutations inside the coding region (red boxes), which is confusing since the authors specifically describe them as 'non-coding' mutations. If you read that as 'mutations that don't change the protein sequence', these could be silent mutations
UTR 3′: in the transcribed region, but not part of the coding region, as shown in the picture (blue box after coding region)
<5 Kb upstream: outside of the transcribed region, but possibly part of an enhancer (yellow boxes after coding region)


Why is the Patellar reflex not triggered when the tendon is extended slowly? I have been previously told that the Patellar reflex (knee-jerk-reaction) exists to prevent the hyper-extension of the patellar tendon.  Yet if the impact to the tendon is delivered slowly - i.e. by pressing down on it rather than striking it - there is no reflex response.  Why is this, as surely the tendon is being extended by the same amount?

This effect you are observing has to do with the nature of the afferent neurons (Ia fibers), which carry a signal into the spinal cord and synapse onto motor neurons directly.  See this text (scroll down to section 1.10) for a diagram.  At their other end, these Ia fibers penetrate into the muscle and wrap themselves around the body of the muscle spindles, "[which] are specialized receptors that signal (a) the length and (b) the rate of change of length (velocity) of the muscle."

Because the main role of these spindles is to monitor the muscles for very rapid changes in length, the neurons have a static range which is optimized for these quick jerks (rather than firing over a wide range of velocities).  When you are stretching the muscle slowly, the Ia fiber is not building up a sufficient depolarization to fire off an action potential.


Giant insects growing question During the dinosaurs time 100-200 million years ago there were giant insects like 1 meter long. An example is here. One of the theories why they could grow this big is that oxygen level was much higher than now. Now we have like 20% oxygen in the air and that time it was 30 or 40.
The question:
If I make a tank/aquarium with 40% oxygen and all the equipment to make this oxygen concentration constant. I put there modern insects, dragon fly, worms, slugs, etc. Will they grow to much bigger size than normal from the 1-2 generations, or I will need to have 100 or 1000 generations before they will be bigger?

that sounds like a fun experiment!  But unfortunately you are right, the size difference is shaped by genetics as well as an environmental condition that might be hard to pin down.
For the genetics, It would indeed take millions of years (or at least 100,000s) for the genetic adaptation to kick in to create that change.
As for the environmental conditions, another source of gigantism is being on an island.  As the small number of species expand to fill out all the niches in the tank, they may get larger simply because the environment allows it with no predators.
The tank would have to be enormous to get those niches I think. This paper describes an archipelago of islands and shows that you tend to get smaller animals more easily with smaller islands, and larger species need larger islands.  Large here is millions of square meters.
Both of these processes take many generations. This is not my field but this paper studied 200 generations of plants and showed only migration and lifespan changes.  Size adaptations that come with changing ecological roles might have to take 1000s of generations. We'd have to freeze ourselves to see the giant slugs.  I'm sure there's a better answer out there, but this is what i found so far.


Why do most breast cancers occur in women? According to Korde et al. (2010):

  Male breast cancer accounts for less than 1% of all cancers in men and less than 1% of breast cancers.

This raises the question: Why do most breast cancers occur in women?

Two plausible explanations I can think of:

A male is less likely to get breast cancer for anatomical reasons (such as a smaller quantity of breast tissue, or breast tissue that is less susceptible to cancer),
Women have higher significantly levels of estrogen, which is linked to mutations that cause breast cancer (see Cavalieria et al. (2006)).

Although, I have no evidence to suggest that either of these is predominant factor.

Yes, this is mostly about estrogen. Most breast cancers rely on endogenous estrogen to sustain proliferation.

Some general reading: Cancer Medicine, Chapter 18

More in-depth reading: Endogenous Hormones as a Major Factor in Human Cancer

Requested summary of mentioned readings:

First of all, there is an established link between breast cancer cell proliferation and concentration of estrogens and progesterone, which is logical, because normal breast cells divide in response to those hormones (e.g. puberty, pregnancy, even luteal phase of the menstrual cycle). Secondly, the incidence of breast cancer in women correlates with major changes in their hormonal profile - girls and elderly women (i.e. women with lower levels of sex hormones) don't get breast cancer.

Many factors, that influence the risk of developing breast cancer are in fact tightly connected to the hormones' levels. For example - early age of menarche (or, more importantly, first ovulation, because physical activity at young age disturbs ovulation AND is protective against breast cancer) and Hormone Replacement Therapy raise the risk, early age of first full-term pregnancy or any form of artificial menopause (such as preventive oophorectomy for women with mutations in BRCA1 or 2) reduce the risk.

The first table from the book chapter lists known risk and preventive factors. The review article explains the same ideas, but connects them to other types of cancer (e.g. ovarian cancer) and suggests mechanisms, which might be the cause of those risk changes.


How could be the "Eurasian magpie" bird won the "Mirror Test" where Gorillas failed EURASIAN MAGPIE VS GORILLA

   VS

How could be the "Eurasian magpie" bird won the "Mirror Test" where Gorillas failed ?

  In 1982, mirror tests on two, zoo-reared gorillas failed to demonstrate self-recognition. The authors wrote "[These studies]...suggest that the gorilla may be the only great ape which lacks the conceptual ability necessary for self-recognition." In 1993, a report was published that although six gorillas had previously failed to exhibit self-recognition.

  The Eurasian magpie is the only bird to pass the mirror test. Researchers applied a small red, yellow or black sticker to the throat of five Eurasian magpies where they could be seen by the bird only by using a mirror. The birds were then given a mirror. The feel of the sticker on their throats did not seem to alarm the magpies, however, when the birds with colored stickers caught a glimpse of themselves in the mirror, they scratched at their throats - a clear indication that they recognized the image in the mirror as their own. Those that received a black sticker, invisible against the black neck feathers, did not react.

  Reference

Birds lacks neocortex, the area where self-recognition was thought to reside. Then which part of the brain do birds like Magpies uses to process these complex cognition ?
Why do Gorillas failed the mirror test ?

I think this website provides a pretty surprisingly thorough breakdown of avian brain anatomy, including historical contexts and debate around what exactly is homologous and what is not, and whether 'homologous' is a useful bit of information.

In short: It was thought until recently that the bird brain was just the core of the mammal brain with some layers peeled off, but it turns out to be more like a scale model, with many of the same parts. Roughly. Sort of.

So birds do not technically have a neocortex. They have a structure that looks like a neocortex, but it also looks like some other things. Gorillas do have a prefrontal cortex etc (even if they are smaller than in humans). The knowledge that structure X performs function Y in an organism generally implies little about a second organism, with or without structure X. Even features like 'wings are for flying' and 'fins are for swimming' have exceptions.


Gene terminology - is one gene a concrete, single physical sequence? Suppose you have two identical copies of the same, coding nucleotide sequence (e.g. two copies of BCL2 - a random gene I found on Wikipedia).

Could you say that these are two genes (i.e. the name "gene" refers to a specific, physical sequence, and where there are two of them, you have two genes, even if identical)? Or just two molecules of one gene (in the same way that when you have two molecules of carbon dioxide, you can't say that they are two carbon dioxides)?

'just two molecules of one gene'.

They are the same gene. Gene is more of an abstract concept. We say for example that humans have ~ 20,000 protein-coding  genes. It does not mean that we have only 20,000 molecules, one for each gene. We have many more molecules of course. What we mean is that we have 20,000 different entities, each coding for a specific type of protein. If you have two molecules of a sequence in a tube, it becomes questionable whether these sequences can be thought of as genes. I would say that those sequences lose their 'genicity' or their property of being genes because they are not coding for anything in a tube. They lack the cellular machinery that makes them code for something. I would just say you have 2 nucleotide sequences of the gene BCL2 but not that you have 2 copies of the gene BCL2. It's maybe just a personal difference I see though.


Is Active Transport Required For Life? Is active transport required for all living cells to function?

I was under the impression that if a cell doesn't have active transport, it either would lose molecules through the membrane and not be able to maintain a proper gradient, or molecules would be trapped inside the membrane (waste) or outside the membrane (food).

For an organism (think single-celled) living in just the right kind of environment, it might just be possible to survive using only facilitated diffusion, at least as far as small molecules are concerned. This kind of organism would have to maintain exactly the right concentration of the molecules it wants to keep or get rid of, based on the external concentration of those molecules.

For example, if an organism was living in a glucose-rich environment, it might be able to fulfill its glucose requirements by (1) making the membrane itself tightly impermeable to glucose and (2) tightly controlling the number of passive glucose transporters.

It would be nigh-impossible to achieve this for every solute in the environment, especially those that are able to permeate the membrane.

If there were such a thing, it might be found in organisms that live in very low energy aquatic regimes such as anaerobic methane oxidizers, where the solute concentration in the environment doesn't really change in small time scales.

Even in such environments, the number of small ions in the environment is likely to be high enough that some active transport would be required to maintain the osmotic balance within the cell.


Burning fat transferred from one part of the body to another While doing some research on cosmetic surgery, I discovered that there are several ways of doing breast enhancements, one of which was using body fat. While I haven't researched this method, I assume they transfer the patients body fat from one part of the body to another.

Would the body use this transferred fat for as energy, or would it ignore it as it wasn't stored there in the first place? Does the body differentiate fat cells stored in different parts of the body?

Would the body use this transferred fat for as energy, or would it
  ignore it as it wasn't stored there in the first place?

It would use it as energy source, there is no such thing as "ignored tissue". Fatty acid mobilization is regulated by epinephrine and insulin. These are hormones which are ofc. carried by blood, so every white adipose (fat) tissue is affected by them.

Figure 1 - FFA and glycerol mobilization - source
2003 - Fatty acid mobilization from adipose
tissue during exercise

  Does the body differentiate fat cells stored in different parts of the body?

This is obvious, just check breasts and butts of girls. ;-) (Those are subcutaneous fat depos. They size is probably regulated by estrogen.)

There are other things involved here, we can talk about subcutaneous (fat below the skin), intramuscular (fat in the muscles) and visceral (abdominal fat) white adipose tissue (there are white, brown and beige adipose tissues). The visceral fat is associated with metabolic diseases, obesity etc...

1995 - Pathophysiology and Pathogenesis of Visceral Fat Obesity
2012 - Lower Thigh Subcutaneous and Higher Visceral Abdominal Adipose Tissue Content Both Contribute to Insulin Resistance
2013 - Genomic and epigenomic regulation of adipose tissue inflammation in obesity

The regulation of body fat distribution and amount is complicated and regulated differently by subcutaneous, intramuscular and visceral fat.

  The total transmissible variance ranged from about 40 percent for the
  amount of subcutaneous fat to 60 percent for the pattern of
  subcutaneous fat distribution. Biological inheritance accounted for
  only 5 percent of the variance for subcutaneous fat and the body mass
  index, but 20 to 30 percent for the percentage of body fat, fat mass,
  fat-free mass, and fat distribution. These data suggest that the
  amount of internal fat is influenced by heredity more than the amount
  of subcutaneous fat. Furthermore, we consistently found that
  nongenetic influences are quite important in determining the amount
  and distribution of body fat in the population.

1988 - Inheritance of the amount and distribution of human body fat

  These data suggest that adiponectin concentrations are determined by
  intra-abdominal fat mass, with additional independent effects of age
  and sex. Adiponectin could link intra-abdominal fat with insulin
  resistance and an atherogenic lipoprotein profile.

2003 - Relationship of adiponectin to body fat distribution, insulin sensitivity and plasma lipoproteins: evidence for independent roles of age and sex

  The FFA storage pathway, which had remained undetected in
  postabsorptive humans until recently, can have considerable,
  long-term, and sex-specific effects on body fat distribution. It can
  also offer a way of protecting the body from excessive circulating FFA
  in obesity.

2011 - Storage of Circulating Free Fatty Acid in Adipose Tissue of Postabsorptive Humans
Quantitative Measures and Implications for Body Fat Distribution

Different colors (white, brows, beige) and orgin (subcutaneous, intramuscular, visceral) originate from different progenitor cells.

  These results reveal a major ontogenetic difference between visceral
  and subcutaneous WAT, and pinpoint the lateral plate mesoderm as a
  major source of visceral WAT. They also support the notion that
  visceral WAT progenitors are heterogeneous, and suggest that
  mesothelium is a source of adipocytes.

2013 - Visceral and subcutaneous fat have different origins and evidence supports a mesothelial source

  Brown and white adipocytes have been shown to derive from different
  progenitors. In this study we sought to clarify the molecular
  differences between human brown and white adipocyte progenitors cells.

2014 - Comparative gene array analysis of progenitor cells from human paired deep neck and subcutaneous adipose tissue

The regulation of fat distribution is under research, and not fully understood yet.

  Fat distribution differs in men and women, but in both sexes, a
  predominantly gluteal-femoral compared with abdominal (central) fat
  distribution is associated with lower metabolic risk. Differences in
  cellular characteristics and metabolic functions of these depots have
  been described, but the molecular mechanisms involved are not
  understood.

2012 - Distinct Developmental Signatures of Human Abdominal and Gluteal Subcutaneous Adipose Tissue Depots


What is correct MVM vs. MMV? I'm writing up a report and I see conflicts everywhere on the internet. Should it be Murine Minute Virus (MMV) or Minute Virus of Mice (MVM).

The followup question is does it really matter.

According to the International Committee on Taxonomy of Viruses, it has had several official variations of that name over the years:

Minute mouse virus
Minute of mice virus
MVM Virus
Minute virus of mice
Mice minute virus

The current (2014) accepted name is: Rodent protoparvovirus 1

"Does it really matter?" As long as you write in full the name you're using the first time you use it, people will know what you're talking about. However, for consistency amongst current literature, perhaps we should all strive to keep up with current taxonomy.


Microarray gene expression matrix format After scanning the microarray chip we get RAW data with different formats depending on the type of microarray used. However, these RAW data files can be normalized and processed to generate gene expression data matrix.

I've been trying to figure out what exactly is the result of the processed data and what is the format of that data. As I've seen so far, there's no specific format for processed data. Of course most of them agree that columns represent experiments and rows represent genes, but the additional information at the top, they're usually different but I'm not sure based on what. Can anyone suggest me with the most common used formats? Is there any additional information to that processed data file in case I wanted to apply classification on it?

The RAW signal values from each microarray are transformed and processed to give you normalized signal values for each microarray. The transformation and processing steps are standard but different for each manufacture. Each manufacture uses a different method/technology to obtain signal values. Thus, signal values are not directly comparable between different microarray technologies.

Experiments using different technologies might get similar RANK of results but the normalized signal values will be different. You can have a look at GEO for a list of datasets and commonly used technologies. I have no clue what you mean by applying classification (are you looking to cluster the results from different microarray technologies run on the same experiment? I'm pretty sure a comparison of microarray technologies has been done before/already)


Why is Artemisinin Compound Therapy preferrable over Artemisinin therapy with regards to drug resistance? How does adding other anti-malarial drugs to artemisinin, to obtain a "combined" therapy result in reducing the frequency of emergence of resistance?

  And it is given in the form of artemisinin combination therapy,
  combined with another anti-malarial drug, with the goal of reducing
  the frequency of emergence of resistance. (Cf source).

The idea is rather simple. When an antibiotic is used, it becomes a driver to select for a mutant that has resistance towards the antibiotic. Let say the probability for that happening is P1 (Lets say 1 in 10, 0.1).

When you use two antibiotics with different modes of attack, the probability of acquiring resistance to both is P1 x P2. (Let say P1 =0.1 and P2 = 0.15). So P1 x P2 = 0.1 x 0.15 = 0.015

Hence the probability of becoming resistant to both antibiotics at the same time is very much lower. And as the antibiotics are always used together, the time a bug needs to develop resistance to the therapy becomes longer. The duration which you can use the drug is increased.


What in the world is this critter? We spotted this thing crawling around a (thankfully empty) bowl in our apartment in Barcelona, Spain. I have never seen anything like it. It appears to be some kind of caterpillar-like insect, but it is inside a flat, leaf-like shell. It can only move by sticking its head out a hole in the tip of the shell and it has to pull itself by its front legs (no legs under the shell). But it can actually pop out of either end of the shell! When it's threatened, it just hides inside the shell completely.

I'm completely flummoxed as to what this thing is. Does anyone have any clue?

(click the images for full-size)

Found it. It's a case-bearing moth larva.