Can dish soap really be used to kill ticks and fleas? An answer at Pets suggested using dawn dish soap to kill fleas. I did a little looking around, and found several references supporting the idea.  Most of what I found was in 'selfhelp' and 'save a dime' type books and web sites. So while it seems to be a popular idea, I am unsure if it is an effective idea.

Is there any reliable science supporting the use of dish soap to kill fleas and/or ticks? If so what points in the life cycle would it be effective?  If it does work, how often would I need to use it to be relatively sure all the fleas/ticks have been through the appropriate life cycle and are dead?

First part of the answer - Yes fleas (Siphonaptera) can be drowned. But not as easily as the internet would lead you to believe.

There are many claims on the internet (and printed works) expounding on how simple it is to drown fleas.  The best science I found so far on the topic is in Forensic Entomology: An Introduction By Dorothy Gennard; John Wiley & Sons, Apr 30, 2013; section 4.3 which reflects a 1985 work by Simpson K. (Journal of the New York Entomological Society 76: 253-265, not finding this online). Gennard is using the fleas present on a human body at death to determine how long the body had been submerged.  Findings -

A flea submerged for up to 12 hours will appear to dead, but can revive in about 60 minutes after being removed from the water
A flea submerged for 18 - 20 hours will appear to dead, but can revive in  4- 5 hours after being removed from the water
It takes 24 hours of full submersion to fatally drown a flea

Side note; lice (Phthiraptera) can be fatally drowned in about 12 hours.

Second part of the answer - Yes soap can facilitate the death of fleas in bathing

So far the best I have is Medical and Veterinary Entomology by Gary R. Mullen, Lance A. Durden Academic Press, Apr 22, 2009

This work suggests the process of washing the flea (and the pet) removes integumental waxes on the fleas body and they die from desiccation (dehydration).

More Research

I have been unable to find solid research specific to fleas (Siphonaptera) and soap (surfactants), so I had to reach in to the general insect works for answers.  There are a number of pesticides which include surfactants in their make up to increase effectiveness but these seem to be to an aid in the delivery of the pesticide not because the surfactant has any additional killing power.

  a surfactant may affect the efficacy of an insecticide by its influence on wetting, spreading and run-off rather than by its influence on cuticular penetration

The Physiology of Insecta, Volume 6 edited by Morris Rockstein

There is some science suggesting soaps can help break down cell membranes but they seem to be most effective on soft bodied insects (which fleas are not)

  Soaps... kill insects by disrupting the exoskeleton and breaking down cell membranes.  Soaps generally work best against small soft bodied insects such as aphids, scale crawlers, meatybugs, and young caterpillars as well as spider mites.

Destructive Turfgrass Insects: Biology, Diagnosis, and Control By Daniel A. Potter

Summary

There are multiple online reports of "drowning fleas" and killing them with soapy water.  After looking for the science there does not seem to be much support for these fatal claims. There is little doubt that giving your pet a soapy bath in the tub will help remove the fleas, they may even appear dead.  But in all likelihood these fleas are just waiting to dry out and be revived, hopefully in the city sewer.  If you bath your pet in the yard, and than let the dry pet in the yard again the next day the clean pet and clean revived fleas will likely reunite. Soapy water is more likely to facilitate removal of the comatose flea from the pet and carry it down the drain. So it is reasonable to have noticeable decrease in the flea population after a bath.  But excessive bathing has it's own risks and given the life cycle of a flea soapy baths alone are unlikely to be a final solution.


Is this answer about the limiting factor correct? The graph shows the result of adding both phosphorus and nitrogen to different algae populations. I have a hard time figuring out why the correct answer is C, I thought that  groups 4 and 5 would have nitrogen as a limiting factor because adding it increases their growth. Help me please.

I agree with you, and think that there is a mistake in the "Correct answer". The interpretation in the "Explanation" seems to be correct though ("Algae at locations 4 and 5 exhibited growth in response to fertilization with nitrogen."), so I think that there is a typo/mistake in the "correct answer". The answer should be D.

Normally within ecology (and especially in reference to nutrients, such as  nitrogen and phosphorus), limiting factor refers to the substance/nutrient that is in short supply within a particular environment, and is therefore limiting the potential growth of organisms. For examples, see any ecological textbook or Blumenthal et al (2001) (as an article example, picked at random). The concept of limiting factors is related to Liebig's_law, which states that growth of organisms is determined by the scarcest resource, and not the total level of resources.

When performing a couple of searches now, I see some instances though where the term limiting factor is used on the opposite way, in reference to toxic substances. One example of this is Imadi et al (2016), where monomeric aluminum reduces root growth due to aluminum toxicity. This is not the most common use of the term though.


Activation Of Embryonic Genome Embryonic gene activation is a process by which the embryo begins to transcribe its newly formed genome.As the embryonic gene activation occurs during early stages the paternal genome may not have any influence at that stage.

Now,
My question is why does only the maternal genome play a role in embryonic gene activation?
Does paternal genome have a role in prior/post embryonic genome activation?

The pronuclei fuse and decondensation happens and now the cell is called a zygote. There is a stage called the midblastula transition (MBT), until which only the maternal products (cytoplasmic factors such as RNAs, proteins and ribosomes) are used. After MBT the zygote starts expressing its own genes from both the paternal and maternal alleles. However, certain genomic regions are imprinted  which means that one of the alleles is epigenetically silenced. It can be either paternal or maternal.


Excercise and fitness in old age I have seen so many news and study online, saying exercise keeps body healthy in old age and keeps us fit? how is this possible normal tear and wear will become more with activity hence more mutation hence more loss. Why exercise help?

Tear and wear means lots of regeneration in our body, regeneration will lead to mutations, no regeneration is perfect, hence more regeneration's, more risk of bad DNA.

Not all "wear and tear" is bad. I will provide only one example. Trust me, I can provide many more, but I think one is sufficient to answer your question.

Exercise (against resistance, e.g. even gravity) is known to strengthen bones, for example. The stronger your bones, the less likely they will break as a result of a fall. While that sounds kinda "meh", it's incredibly important in the elderly, because once they sustain a fracture, their activity level falls dramatically for fear of sustaining another fall/fracture. Because of this, they have a decrease in muscle mass, a decrease in lung capacity, a decrease in cardiac fitness and an overall acceleration in decline of motor function, as well as a decreased quality of life.

  Low-impact fractures, commonly called fragility fractures, have even higher mortality. Older patients with injuries from a fall have five times the mortality that their same age colleagues have from injuries from MVCs (motor vehicle accidents.) Five-year survival after an osteoporotic hip fracture is similar to that of patients with breast or other cancer. Almost one in 13 (7.5%) of those with fragility fractures will die within 90 days of fracture.* ...A fracture can be a devastating blow to an older adult’s health and independence, decreasing functional status and quality of life permanently. While some may recover their independence, half of older adults will require home health care in the 6 months following a fracture, and many will have long-term functional decline.

"Wear and tear" is good for muscles, bones, the heart, the lungs, balance, proprioception, and a number of other systems which help to prolong life, as well as the quality of life.

*Mortality is mainly with regards to hip fracture.

Fractures in Older Adults


Is Schoons Hard Shell muskmelon a hybrid? Would Schoon's Hard Shell muskmelon be considered a hybrid as I have read it was a cross between a Bender's Surprise and a Honey Rock.

Goldman surmises that Schoon's Hard Shell is a variant of the Bender, so would have been bred from the Surprise, Irondequoit, and Tip Top, all of which were from the Sill's Hybrid.
In that sense, I suppose it's a hybrid. I'm guessing that you're asking because you want to know if you can save the seed; that is, if Schoon's Hard Shell will breed true or will lose its characters in subsequent generations.
I can't find any specific detail on that, but given that it's sold by Seed Savers Exchange, I'd guess that it is a good candidate for seed saving, as long as you make sure it's not crossing with related species in your garden. Seed to Seed has detailed info on melon seed saving.

Goldman A. 2002. Melons. Artisan Books (p. 76)

Whealy K. 2012. Seed to Seed. Chelsea Green Publishing (p. 103)


Why upper surface of leaves is more green and shiny than the lower one? I have properly googled this and got various answers. However, those answers do not provide an answer to the "Why" part of my question. Why is it that the upper surface of leaves is more green than the lower one? Some sites suggest that it is because of the thick cuticle. Yet, that sounds weird and doesn't fully convince me. What other reasons to why the upper surface of leaves is more green and shiny than the lower one, could there be?

You can find two chlorophylls in most plant leaves, chlorophyll a and b. We'll use as a reference Leaf characteristics and chlorophyll concentration of Schyzolobium
parahybum and Hymenaea stilbocarpa seedlings grown in different
light regimes. The most important observation is that in shade-tolerant leaves, chlorophyll b dominates chlorophyll a. And the opposite is true of shade-intolerant leaves. I'll argue now that the portion of a given leaf that must tolerate more shade will have the darker green pigment due to the presence of more cholorphyll b, and that the side of the leaf that must tolerate lots of light will have the lighter pigment due to the presence of more chlorophyll a.

The light-tolerant side of the leaf is also shiny, and this is because of a thick waxy cuticle. The shade-tolerant side of the leaf also has a cuticle but if we follow it logically, the light-tolerant side of the leaf needs more protection from heat evaporation because it's always being hit by light.

So what I'd do, instead of thinking of the leaf as having a top or bottom, think of them as having a side that must tolerate excessive shade, and a side that must tolerate excessive light.


DNA extraction from oil-containing seeds Which protocol of DNA extraction from plant oil-containing seeds take fast and good result in purity that can use in RT-PCR(Real Time polymerase chain reaction)?

The paper "Modified method for combined DNA and RNA isolation from peanut and other oil seeds." has a nice protocol for isolating DNA and RNA (which later can either be differentially digested or precipitated) from oil seeds for PCR. You can find the complete paper in the link above, the materials and methods sections says the following for the extraction method:

  RNA and DNA isolation

  Approximately 1–1.2 g of dried seed of each genotype was utilized in
  extraction. Seeds were frozen with liquid nitrogen and pulverized by
  grinding with mortar and pestle until a fine powder. Tissue was placed
  into 10 mL solution I (100 mM Tris, 150 mM LiCl, 50 mM EDTA, 1.5 %
  SDS, 2 % PVP-40, 1.5 % b-mercaptoethanol) buffer, pH 7.5, and mixed
  thoroughly by vortexing or inversion.

  To the homogenized tissue, a 5
  mL acid phenol, pH 4.3 (Fisher Scientific, Pittsburg, PA) was added
  and tissue was mixed thorough for 5 min, followed by the addition of 5
  mL chloroform:isoamyl alcohol (24:1) and mixed for an additional 5
  min. The homogenate was centrifuged for 10 min and the upper aqueous
  layer (around 9 mL) was transferred to a fresh 40 mL tube containing 9
  mL of solution II (2 M guanidinium thiocyanate, 0.5 M sodium citrate,
  1.5 M ammonium acetate, 1 % N-lauroylsarcosine) buffer, pH 5.2, mixed by gentle inversion, and allowed to incubate for 10 min at room
  temperature.

  After incubation, a 4.5 mL phenol:chloroform:isoamyl
  alcohol (25:24:1), pH 6.7 was added, mixed thoroughly for 5 min,
  centrifuged for 10 min at 13,000g, and the aqueous layer (around 16
  mL) was transferred to a new 40 mL tube.

  To the transferred solution,
  9 mL 1.2 M NaCl and 9 mL isopropanol were added, mixed, placed on ice
  for at least 1 h, and centrifuged for 15 min at 13,000g. The liquid
  was discarded and the resulting pellet was washed with 2 mL cold 70 %
  ethanol, dried, and resuspended in 4 mL RNase-free water.

  4 mL 4 M
  LiCl was added, mixed, placed on ice in the refrigerator for at least
  1 h, and centrifuged for 15 min at 4°C at 13,000g. The supernatant
  (around 8 mL) was transferred to a new 40 mL tube for DNA isolation
  and the pellet was retained for RNA isolation. For RNA isolation, the
  pellet was washed with 2 mL ice-cold 70 % ethanol, dried, and
  resuspended in 750 lL RNase-free water.

  For DNA isolation, 8 mL
  isopropanol was added to the transferred supernatant tube, mixed well,
  centrifuged for 5 min, discarded the liquid, washed pellet with 2 mL
  ice-cold 70 % ethanol, dried, and resulting pellet was resuspended in
  500 lL 10 mMTris, pH7.5. The amount of DNA or RNA was determined using
  Nanodrop 2000c spectrophotometer (Thermo Scientific, Wilmington, DE).


What does z in lac z, y in lac y and a in lac a gene stand for? In lac operon the 3 structural genes lacz, lacy and laca must have some reason behind their names. While lac refers to lactose but what does z, y and a refer to?

The Jacob and Monod article on regulation is paywalled, but there do seem to be some PDFs floating around.
In this article, the terminology of z and y is introduced as designators for mutants (z+ and z-, y+ and y-).

The z appears to be linked to a term from a kinetic equation.
The y is not justified, implying that it is an arbitrarily chosen variable, and such choices are often by convention adjacent to the justified variable (e.g., the index variable i is often followed by additional indices j and then k).

The a component is not present in the original article, but its name seems likely to come as an abbreviation of its function as an acetyltransferase


Why do simulations of dichromatic color vision portray medium wavelengths as yellow rather than green? Please take the time to read & answer this at your own convenient pace.

Is this even the right way to put this?

Do you think this post better belongs in the Physics or Philosophy forums?

This must be part of the old philosophical question of whether you see the same colors as I do.

This is a simple question really, but the description may get a bit technical if your not familiar with the basics. If you find this complicated to read then I can write it more basically if you desire.

It’s important to bear in mind that we shouldn’t equate or compare other animals’ senses & perceptions with our own, such as ‘modified’, ‘enhanced’, ‘dehanced’, ‘reduced’ or ‘increased’ human senses.
We can form educated estimations about how the perception of other animals is through study of their nervous systems, brain & sense organ anatomies & behavioral tests, but have little way of proving how they actually experience things.
The same applies to other humans, only that we have more ways of proving how other humans actually experience things because we have language, but even that’s still very subjective.
It’s a basic fact that unlike shape, dimension & location, sensations are not matter & energy itself, but our brain & mind’s representation of them. For example, how do we know for sure whether other animals even perceive gradients of light as shades of black & white? It could turn out to be something totally different, even uncomparable or unimaginable for us.
This is common sense when mentioned, but many people forget or aren’t aware of this basic fact to keep in mind.

Nevertheless, what I’m wondering is whether the short-medium wavelength dichromats of most mammals & some humans & New World Monkeys, which have two kinds of opsins sensitive to short & medium visible EM wavelengths in constrast to having the extra opsin sensitive to long visible EM wavelength for most humans & anthropoid primates, actually see green or yellow as their primary color representating the middle EM wavelength?

Simulations of dichromatic color vision usually portray them as seeing the primary colors blue & yellow, with the rest being combinations of those primary colors & shades of black, grey & white.
In fact I’ve never come across a dichromatic simulation using green to portray the perception of the middle wavelength color for them.
Its always yellow.
Could it be because we’re not exactly sure whether short-medium dichromats actually see either green or yellow as their primary color for middle wavelength peak, if they even do see those colors for that matter?

However, yellow is not a primary color. It may be in art & design, but it’s not in biology & physics.
Yellow is the extreme end of red & green, & a mixture of red & green.
In biology & physics, red, green & blue are the primary colors.

So what I’m wondering is why do simulations of dichromatic color vision portray the perception of the medium visible EM wavelengths in gradients of yellow rather than green, the actual primary color for middle visible EM wavelength, & how can we know or give the best answer to what color dichromats see as their perception of middle wavelength of Visible EM?

So which color is it? Yellow or green?
& is it the same for all short-medium wavelength dichromats?

How would we know? If we can’t, then what is the best evidence & way to give the best educated guess?

Like why is the dichromatic simulation of the frog & parrots below using yellow & blue to represent their primary colors? Wouldn’t using blue & green be more honest to biology & physics? Isn’t yellow not a primary color but the extreme end of & mixture of both red & green?

Opponent color processing.

https://en.wikipedia.org/wiki/Opponent_process

Studies have shown blue and yellow are opponent colors, as are red and green. We process the colors in opposition, as in perceiving one requires perceiving less of its opponent, equal amounts of both (minus other colors) yields no color in your final visual perception. If you cannot differentiate red and green, than the only two colors you can differentiate reliably are yellow and blue. As a side note this is also why in image processing programs these colors are on paired sliders, it is the simplest way to manipulate color images.

The most common forms of color blindness in humans, and the one all non-primate mammals have prevents them from differentiating red and green.

If you cannot differentiate red and green, and if I show you blue and yellow, you see no color, if I show you red and green you see yellow, becasue your blue cone is not being activated.

The image below is our opponent pairs in our vision.


Why do we need to grow plants to make food? Why can't we synthesize the nutrients that we need directly from chemical reactions, from energy and simple inorganic molecules found around us? If it's hard, why not try to copy how plants do it?

I feel like growing plants is very inefficient: it is consuming a lot of energy for intermediate steps that may not be required – growing roots or inedible parts, performing reproduction, consuming soil and space, requiring constant light and irrigation... And huge amounts of energy is invested to slightly compensate for these caveats and increase productivity, while it still looks like an inefficient way of doing synthesis of nutrients and other compounds we need to eat.
Is there a reason that such resources are not directed to building processes to perform such synthesis via other – hopefully more efficient – means than growing plants/animals?

Note that I found a partial answer there, however I was not satisfied by an unexplained "photosynthesis is the only viable way to create material that can yield those nutrients".

Is photosynthesis that hard? If that so, why?

If it's so hard using organic chemistry, why cannot we simply extract/mimic the biological reactions happening in the plants to generate nutrients? (we still don't need to grow whole plants)

If we are not able to do that, what does it means about our current understanding/mastery of chemistry and biology ?

We are part of a biological system, and we evolved to be part of it. Plants are the base of that system, and the main means of capturing energy and inorganic compounds and converting them to nutrients which are bio-available, along with bacteria.  The further we move from the niche we evolved to occupy, and the further we change the environment of the rest of the system, the more likely we are to bring about our own extinction.
Edit: This answer is somewhat opinion based. We haven't finished the experiment that proves this thesis, yet.


Information and image of Genus Acesina I am searching for image and information, like distribution etc of the genus Acesina. The Taxonomic tree is:

Kingdom:        Animalia
Phylum:         Arthropoda
Class:          Insecta
Order:          Lepidoptera
Superfamily:    Papilionoidea
Family:         Lycaenidae
Genus:          Acesina

According to Catalogue of Life this genus has the 4 species. I haven't found any information by searching web, even the species are extinct or not! Any pointer would be appreciated.

The genus Acesina has been revised and is now part of the genus Arhopala. The wikipedia page for Arhopala has some additional information on this genus.


Why are vegetables either red or yellow? Have you ever wondered why these two colors occur so often? Take these:
onion
waltnut
potato
carrot/parsley
and even cabbage which can be green or red.

Why these two pigments? Or is it just one pigment and it's just its concentration that makes the difference?

Thanks for any explanations!

A lot of fruit and veg are green when unripe and become brightly coloured when they are ready to eat (obviously not true for all, but most fruit/veg does).

This is probably deliberate as a mechanism to signal to birds and animals that it is ready to eat, so that they can disperse the seeds inside.

Red and Yellow are bright colours not usually seen on plants except of fruit/veg, and flowers (which are brightly coloured to attract bees and whatnot), so it makes sense these could be used as signals.

http://www.rosincerate.com/2015/07/colour-changing-fruits-and-veggies.html


Can you get enough water by eating only fish? Scenario: In a boat in the middle of the sea, no freshwater or food stores, no desalination equipment, no rain, but you can catch fish and eat it raw. Can you get enough water this way to survive, let's say for 14 days? (Enough clothes to protect against cold, shade available)

2, 000 g of raw Pacific cod contains 1,650 mL water, 350 g protein, 2,200 mg sodium (source: usda.gov)

By my calculation, you would need to excrete 2,800 mL of urine to excrete urea from protein metabolism (8 mL urine per 1 g protein; source: nap.edu), so after eating fish you would be in the negative water balance for more than 1,150 mL solely from urea.

My questions are strictly about fish as a water source, not about other water sources or survival time:

Does protein really expel so much urine that makes fish an inappropriate source of water?
Any other appropriate source of water from fish, apart from eyeballs? Can you somehow squeeze the water from fish?

If you have a man in a box scenario where you only look at numbers, the answer is, no, he won't last 14 days.[1]

The difficulty with this question for me is that the body doesn't always behave the way it's supposed to. The 3-3-3 rule (3 minutes without air, 3 days without water, three weeks without food) and the "100 hour rule" (4.166 days) aren't absolutes.[2] Some people die in hours, some 10 days. The variables are too great.

Guinness World Records puts the record for survival without water at 18 days[3] by an 18 year old male forgotten in a cell by the police. But he was in a cool basement, and licked the walls which had a small amount of moisture on them. Had he been sweating or 2 decades older, he probably wouldn't have lasted as long.

Water requirement under extreme circumstances varies. How much clothes is your male wearing? Does he have shade? Where in the ocean is he? How inactive can he be? Can he oil his skin with fish oil? But mostly, does he have a still suit (j/k)? These things all matter.

Eating protein without water isn't wise. Carbs are better, but your guy doesn't have them. The better thing for your guy, who can certainly live for 14 days without food, is to suck the water out of the fish, and what he can't suck out, wring out at the end. If he has access to the whole fish, the eyeballs and the spine also have water in them.* The body has all kinds of homeostatic mechanisms to preserve fluids, including continuous secretion of ADH (Anti-Diuretic Hormone), osmoreceptors and baroreceptors to regulate fluid volume and how much water is lost from the kidneys.[4] He'll suffer terribly; fluid will be sucked out of his joints and cells and his blood urea nitrogen will go up and his kidneys will be damaged, he'll hallucinate, he'll need hospitalization, but might he live? If he is young, healthy and hydrated going in, and other factors (a tarp for shade, etc.) mitigate his water loss, I think the answer is yes, he might.

*In 1953, a French physician and sea survival expert, Alain Bombard, set sail in a Zodiac inflatable dinghy with the only food and water officially sealed to discourage himself from using it. He started immediately with drinking small amounts of seawater, and would suck water from fish, and, if he had any fresh rain water, would eat raw fish. He sailed from Minorca to Barbados, eating supplied food and water only once. His rival survivalist, another physician, Hannes Lindemann, contested Bombard's claims, but did well at sea as well.
[1] The Biology of Human Survival : Life and Death in Extreme Environments
[2] Dehydration
[3] Andreas Mihavecz
[4] Fluid Physiology, Ch. 5, 6


How are the dominance and additive effects reflected in the mean and variance of the offsprings of two individuals with known phenotype? If I estimated the genetic additive σ2A, genetic dominance σ2D and environmental effect σ2E of a trait in a population, what will be the predicted value of the offsprings of two individuals with known phenotypes?

My understanding: given that the two individuals are not close siblings, and that the mean of the two parents is μparents, the offspring will have a mean of:

μoffspring = μparents + μparents x σ2D

and the variance will be the environmental variance,  σ2E

How the additive effect  σ2A plays a role in a single mating ? (assuming thousands of offsprings (like in some plants) )?

What is the expected phenotypic trait of an offspring given the phenotypic trait of its parents?

The expected trait of the offspring is equal to the mean of the parents traits.

For this I assumed we don't have more information about the genetic of the trait (typically, without knowing the directionality of dominance and number).

  What is the expected phenotypic trait of the offspring population given the phenotypic trait of the parent population?

As a consequence of the above, the expected mean phenotypic trait of the offspring population is equal to the mean of the parent population (in absence of selection).

  What is the expected variance in the offspring population?

No drift, no selection

In absence of drift and selection (and environmental changes), the variance of the offspring population equals the variance of the parent population.

Directional selection only

In presence of directional selection, please have a look at How does Natural Selection shape Genetic Variation? and ask follow-up question if needed.

Drift only

In presence of drift only, the heterozygosity is reduced by a factor $\frac{1}{2N}$, where $N$ is the population size. The loss of genetic variance is then dependent on (1) the frequency, (2) the dominance and (3) the effect size of alleles at loci causing this genetic variance. There is therefore no simple answer. The only generalization that can be done is that (1) the expected variance of the offspring population is lower than the variance of the parent population and (2) the smaller the population size, the higher is the expected loss of genetic variance

General Note

My feeling about quantitative genetics (but I am not really an expert in that field) is that it is often frustrating to see that generalization is often impossible and general solution to recursive equations often don't exist implying that predictions to more than one generation must be calculated through iteration.

I suspect that an expert in quantitative genetics would be able to say much more than me in this post.

The book Introduction to Quantitative Genetics (by Falconer and Mackay) is probably still the best book to increase your knowledge in quantitative genetics.


Evolution of Heteromorph Ammonites I was reading about fossils and thought of this question: what was the purpose of the shells of heteromorph ammonites (for example, ammonites of the genus Nipponites)?
Wouldn’t the odd shapes of these shells cause more drag? So why did their shells evolve to be that way?

I'm not an expert in functional paleontology, but it has been suggested that the specific shape of heteromorph ammonites could be related to hooking on to macrophytes or branched animals:

Examination of ribbing pattern and its resolution in various parts of
the living chamber in 11 species revealed that the ribs were less
developed and had some traces of wear on the inner surface of the
hooked chamber, being well developed both on the lateral and outer
lower parts. This could indicate that the adult animals were
semi-loosely hooked (Ancyloceras, Macroscaphites) or permanently
clipped (Scaphites, Hoploscaphites) onto either horizontal or upwardly
angled stipes of non-calcified algal macrophytes or branched animals.
Comparison of the adult mode of life with those of modern cephalopods
suggested that ammonites of the suborder Ancyloceratina had developed
a stationary brooding phase that could have several ecological
advantages over free-swimming monomorph ammonites.


What pigment is responsible for the formation of blue skin color in some animals? Not long ago I read about Vervet monkey. Here's picture:

My question is what causes this blue coloration of the scrotum? I don't mean evolutionary need  (e.g. attracting females), but what pigment or other factor is responsible for this color?

Blue coloration in animals is caused by structural color rather than blue pigments. In the case of vervet monkeys and other mammals studied this is due to collagen fibers in the skin being arranged with a regular spacing that results in blue wavelengths constructively interfering while other wavelengths destructively interfere1.

This "news" article in Science discusses this phenomenon and mentions Vervet monkeys.

Reference:

1: Prum, R. O., & Torres, R. (2004). Structural colouration of mammalian skin: convergent evolution of coherently scattering dermal collagen arrays. Journal of Experimental Biology, 207(12), 2157-2172.


Double mutant analysis with null mutants My professor was talking about double mutant analysis with null mutants, and how double mutant analysis won't work with hypomorphs.  I really don't understand the concept of double mutant analysis.

He was talking about pathways - if A and B are in the same pathway, then you would mutate A and he said something about the phenotype being identical.  If A and B are in different pathways, you could mutate both of them and there would be a "stronger" phenotype.

He also said it would only work with null mutants, not with hypomorphs, because with hypomorphs some of the pathway would still be active, not completely shut off.

I really don't understand any of this - what a double mutant is, the whole pathway thing, why the phenotype is "identical" or "stronger", or why you use hypomorphs.  I would really appreciate a rundown on the idea of double mutant analysis because my professor's explanation was so unclear.  Thanks in advance.

What is a double mutant ?

See this image.

In this mutant 1 has one mutation, mutant 2 has another mutation while the double mutant has "double"  or 2 mutations.

Key : A,B means double mutation , A means mutation in A and B means mutation in B.

Types of double mutations

  a)Additive phenotype:  A, B = A + B   Implies that A and
  B function independently and on different processes.
   Eg.  A =
  short roots, B = no root hairs A, B = short roots with no root
  hairs.
  Conclusion: A and B function independently on different
  aspects of root development (A is required for normal root growth
  and B is required for root hair development.

  b) Epistatic phenotype: A, B = either A or B

  i) If A = B = A, B   then epistasis implies that both genes function in the same pathway and that each gene is essential to the process.   Eg. A = short roots, B = short
  roots A, B = short roots.  Both A and B are  required for
  normal growth of roots.

  ii)         If A is opposite in phenotype to B, and A, B = A, then epistasis implies that  A and B are in the
  same pathway and B is a negative regulator of A.   Eg. A = long
  roots, B = short roots A, B = long roots.  A is required to
  suppress root growth and B is a negative regulator of A.

  c)
  Synergistic phenotype: A, B >>> A or B.

  Implies that A and B contribute independently to the same process.   Eg. A = long roots (wt = 2 cm, A = 4 cm)    B =
  long roots (B = 4 cm)  A, B = very long roots (20 cm).  A and
  B negatively control root growth independently of one another and
  are performing partially redundant functions.

When your professor was saying that if A and B are in same pathway and you mutate A and phenotype comes as if both A and B have been mutated, then he was probably referring to the epistatic phenotype.

When he was talking about having a stronger effect by mutating them both, he was talking about Synergistic phenotype.

Source : Double mutant analysis


Sleep deprivation relation to growth rate and mental health in adolescence Do sleep deprivation and its timing affect growth rate and mental health in adolescents? If so how much sleep is enough for teenagers?

A couple of papers (from the same group, it seems) defines sleep deprivation in adolescents as less than 6hr of sleep within a month. They found that sleep deprivation increases health risks, importantly depression (which in turns increases sleep deprivation).


Calculating pairwise Fst from allele frequencies I am trying to refresh my memory on population genetics for a project, and I'm having some trouble.

Assume I have genetic data on 3 populations with 5 individuals in each of a given species, with the following number of genotypes:

      0101 0102 0202 0103 0203 0303 0204
Pop1   2    3    0    0    0    0    0
Pop2   1    1    1    1    0    1    0
Pop3   1    0    3    0    0    0    1

I have named alleles 01-03. So 0101 is a homozygote individual for allele 01, 0102 is a hetorozygote individual etc.

Is it possible to do this, from the following formulae:

If I input the information above into Genepop to calculate pairwise Fst using the following dataset:

Test Genepop
TestLocus
pop
Pop1, 0101
Pop1, 0101
Pop1, 0102
Pop1, 0102
Pop1, 0102
pop
Pop2, 0102
Pop2, 0103
Pop2, 0303
Pop2, 0101
Pop2, 0202
pop
Pop3, 0101
Pop3, 0202
Pop3, 0202
Pop3, 0202
Pop3, 0204

it produces the following result:

Pop    1       2
2    0.0278
3    0.2308   0.0669

However, how can this result be reproduced and calculated by hand?

The original Wright's formulation
$$Fst=\frac{var(p)}{\bar p}$$
, where $\bar p = \frac{1}{J} \sum_{j=1}^J p_{j}$ and $var(p) = \frac{1}{J}\sum_{j=0}^J (p-\bar p)^2$ is the variance in frequencies among populations.
This original formulation is valid only for a bi-allelic locus. Nei (1973) generalizes this definition to loci that have more than two alleles.
Nei (1973) general formulation
I recommend to have a look a the paper (Nei 1973), it is a really nice paper.
Nei shows that defining that within Subpopulation gene diversity (a.k.a. expected heterozygosity) $H_S$ and the Total gene diversity (a.k.a. expected heterozygosity) $H_T$ as
$$H_S = \frac{1}{J}\sum_{j=1}^J \frac{1}{I}\sum_{i=1}^I p_{ij}^2$$
$$H_T = \frac{1}{I}\sum_{i=1}^I \left(\frac{1}{J} \sum_{j=1}^J p_{ij}\right)^2$$
, where $I$ is the number of alleles and $J$ is the number of populations. Then Wright's definition of $F_{ST}$
$$F_{ST} = \frac{var(p)}{p(1-p)}$$
generalizes (for cases with more than one allele) into
$$Fst = \frac{H_T-H_S}{H_T}$$
Have a look at Nei 1973 to understand why they are equivalent.
Weir and Cockerham (1984) formulation for several loci
Averaging $Fst$ over several loci is more complicated than one would expect at first place. The solution is given in Weir and Cockerham 1984.
The formulation is a little cumbersome so I just invite you to have a look at the paper.


Why is heart failure treated as more critical than kidney failure? The heart pumps the blood to supply tissues and kidney always filters the blood to remove urea,extra water and etc. And all these are vital,so the kidney is as important as heart:
and my question is:
Why is heart failure treated as more critical than kidney failure?

I don't know that one is treated as more critical than the other. Both are potentially life-threatening conditions.

One in five people over 40 will develop heart failure (HF). That makes it a very common disease of aging, and as more people survive other events (e.g. MI), it will continue to be prevalent, if not to rise.[1][2]

When a patient presents with heart failure (HF), whether it is to a PCP, an urgent care center, or the ER, it is treated.

In the US, the prevalence of CKD (chronic kidney disease) in people ages 60 and older approximately the same as of congestive heart failure (CHF): 18.8 to 24.5 percent. Between 1980 and 2009, the prevalent rate for end-stage renal disease (ESRD) increased nearly 600 percent, from 290 to 1,738 cases per million.[3]

When a patient presents with renal failure (RF), whether it is to a PCP, an urgent care center, or the ER, it is treated.

That makes both conditions much more common (and less emergent) in presentation than, say, anaphylaxis (life-threatening allergies).[4] Known rates or cases of anaphylaxis were 0.0004% for food (e.g. peanuts), 0.7% to 10% for penicillin, 0.22% to 1% for radiocontrast media, and 0.5% to 5% after insect stings.

Emergencies are emergencies, and are triaged for care based on risk, with standardized acuity scales that have five levels (e.g., 1- resuscitation, 2- emergent, 3- urgent, 4- less urgent, 5- nonurgent).[5] To claim that one is treated as more emergent than another, one would need to present evidence that, e.g. HF is rated as emergent more often than RF.

[1] Lifetime risk for developing congestive heart failure: the Framingham Heart Study
[2] Chronic Heart Failure: Contemporary Diagnosis and Management
[3] Kidney Disease Statistics for the United States
[4] Anaphylaxis in the United States
Considering the 1999 US population of 272 million, the population at risk for anaphylaxis from food is 1099, from penicillin is 1.9 million to 27.2 million, from radiocontrast media is 22 000 to 100 000, from latex is 220, and from insect stings is 1.36 million to 13.6 million. These calculations yield a total of 3.29 million to 40.9 million individuals at risk of anaphylaxis.
[5] Emergency Severity Index (ESI): A Triage Tool for Emergency Department


Why can blood vessel contraction be described as a second order system? Suppose that the x-axis represents time, and the y-axis vessel diameter.

Then this graph is claimed to roughly describe what happens when the blood pressure increases, then decreases.

When the blood pressure first increases, the vessel diameter expands to its maximum radius. Then it contracts. What I don't understand is why it keeps on expanding and contracting after its initial expansion - does this model still make sense after its initial expansion and contraction?

Can anyone explain?

Many systems have this property. The plot you are looking at is the plot of the transfer function for blood vessel diameter vs time. A trick in mathematics or engineering is to understand a system is to sometimes look at at different system with the same properties that you do understand. For instance, a mass springer damper system is similar to a RLC circuit. That is, if we understand the mass spring damper system, we view the RLC circuit as the analog to the mechanical system and vice versa. In the case of blood pressure, we also have a driven force (the heart). Thus, an extremely simple model would be
$$
m\ddot{x} + c\dot{x} + kx = F(t)
$$
As we see below, the mass spring damper model produces the a similar plot of the transfer function. If you understand the mechanical system or RLC circuit, you can look at your plot parameters as an analog to one of these systems to understand the dynamics occurring in the body.

A more interesting question is can we use PID control to manage the overshoot, rise time, and settling time of the vessel diameter in the body?

The differential equation that models this process is probably related to a Bernoulli differential equation.

http://en.wikipedia.org/wiki/Bernoulli%27s_principle
page 15 http://www.physics.usyd.edu.au/~jbryant/Fluids/Fluidslect4.pdf
http://bme.ccny.cuny.edu/faculty/bfu/blood%20flow%20permeability%20in%20microvessels.pdf

A precise differential equation will need to account for pressure (Bernoulli), fluids (Navier-Stokes), and the elasticity of the vessel walls.


How come our thyroid glands don't suffer awful mutations (or do they)? I was listening to a lecture by my Biology professor and he said that the thyroid gland contains radioactive Iodine which can break down and create reactive Oxygen species (because ionizing radiation from the Iodine interacts with water in the human body).

So, shouldn't the thyroid gland suffer awful double-stranded chromosomal breaks constantly? Shouldn't we be suffering mutations in the thyroid gland all the time?

Thanks!!!

Radioactive does not mean much in and of itself, your bones are radioactive (potassium), just being radioactive is not enough to do any damage.  It needs to be the right type of radiation and have high enough intensity before it can start damaging DNA and thus cause cancer. Second the amount of iodine in the body is miniscule, the aforementioned radioactive potassium in your body is orders of magnitude larger (if there is any radioactive iodine present at all which is unlikely).

On top of this remember we are surrounded by low dose radiation all the time so our bodies have evolved ways to handle minor damage.http://imgs.xkcd.com/blag/radiation.png


What's the minimum, if any, concentration of atmospheric nitrogen needed by plants? What's the minimum, if any, concentration of atmospheric nitrogen needed by plants?  Would plants be able to grow in an atmosphere with just carbon dioxide and oxygen?

Zero if you are supplying them with solid nitrates in their growth medium, plants can't use atmospheric nitrogen. Some soil bacteria can and create nitrates the plants can use but this can and often is supplied by other means.

But as Graham points out you will need another inert gas to fill in the atmosphere as high concentrations of CO2 or Oxygen are both toxic.


Taxonomy: Categorising Collembola Observe: In some rows (Order, Family), the third column reveals a discerning physical characteristic or body type (Elongate, Slender).

What are the discerning characteristics, missing from the other rows (Superfamily, Subfamily, Genus, Species)?

Basically I want this knowledge so I can work towards being able to separate, categorize (catalogue) and/or identify new or unknown species, etc.

Imagery

Exhibit A

Entomobrya unostrigata
(aka. Cotton Springtail)

Taxonomy

Domain      | Eukaryota        | (Eukaryotes)
Kingdom     | Animalia         | (Animals)
Phylum      | Arthropoda       | (Arthropods)
Subphylum   | Hexapoda         | (Hexapods)
Class       | Collembola       | (Springtails)
Order       | Entomobryomorpha | (Elongate)
Superfamily | Entomobryoidea   |
Family      | Entomobryidae    | (Slender)
Subfamily   | Entomobryinae    |
Genus       | Entomobrya       |
Species     | Unostrigata      |

Sources:
Image; photographed by myself. Text; transcribed from my own hand-written notes. Most likely (originally) gleaned and adapted from publicly available, online information. It may contain errors or inaccuracies.

Resources: Check out Bugguide.net and Collembola.org.

Reprise

Okay, the question has been put on hold, preventing answers from being posted (very irritating and obstructionist policy for those seeking answers, I might add). So I will attempt to clarify.

Exhibit B

Orchesella cincta

Exhibit C

Willowsia nigromaculata

Exhibit D

Entomobrya multifasciata

Exhibit E

Seira bipunctata

The diversity of these specimens; span not only multiple species, but multiple genera. Yet, despite the fact that they each exhibit relatively distinctive combinations of patterns and colours across their cuticle (epidermis, surface epithelium), setae, scales, etc. they all look pretty much identical.

This seems to be the equivalent of declaring a homo sapiens of African descent; a different species to a homo sapiens of Irish descent, on account of their superficial aesthetic differences (most notably regarding melanin; the pigments that determine the colours of a human's skin, hair[s], and iride[s] (eye[s]), and so on). Which, at first seems absurd. But for those of you who disagree, observe the differences between (for instance): Exhibit X vs Exhibit B & Exhibit Y vs Exhibit E. Similar variations between individuals of the same species are not uncommon in the least.

Thus, my question: What are the discerning taxonomical differences between various species and genera of the Arthropoda known as Collembola (aka Springtails)?

Exhibit X

Orchesella cincta

Exhibit Y

Seira bipunctata

The third column doesn't contain distinguishing characteristics at all -- they are the first word of the vernacular (or common) names for those groups on Bug Guide. Specifically, Bug Guide lists order Entomobryomorpha as Elongate-bodied Springtails, and family Entomobryidae as Slender Springtails -- so I think you're just looking at truncated data that's misleading you!

What you're looking for a taxonomic or identification key, which gives you set of yes-or-no questions that will allow you to identify an individual to a particular taxonomic group. Know Your Insect has a taxonomic key that allows you to identify insects to order Collembola, which provides exactly the sort of distinguishing characteristics you're looking for: "This illustration shows two characteristic features of members of this order: the collophore (center), a tube-like structure used to secrete fluids; and the furculum (lower left arrow)." Note that this resource refers to this group as an order, not a class -- that's not uncommon among different taxonomic resources. Wikipedia refers to this group as subclass Collembola!

Unfortunately, it doesn't look like there's a freely available taxonomic key for species within this group, unless you buy a specialized guide like A Key to the Collembola (Springtails) of Britain and Ireland.


Is brain plasticity such that we can train ourself to see with our ears? I am finishing writing some code which will parse a photo (eventually video) and use all the RGB information to synthesize an audio representation. I am wondering whether a typical person has sufficient neural plasticity to learn how to listen to this audio to understand an image in a general sense? I am not looking for perfection.  If the person has good vision they would do well to spend time listening to such synthesized audio while simultaneously viewing reality to give some training to enhance their interpretative abilities.  Once trained they could augment or supplant vision with its sonic equivalent.

  How plastic is our audio-visual brain? Is there hope this will work ?

PS.  Once working I will update this Q

For those wondering about the details :  I am traversing the image using a Hilbert Curve which tends to preserve spacial relations amongst pixels to minimize re-training upon change to pixel resolution.  This flattens the 2D photo into a 1D line sprinkled across from left to right with points storing respective pixel values (at a 1st approximation I collapse RGB into grayscale 0.21 R + 0.72 G + 0.07 B)

... to create the audio representation I visit each pixel position on this line and introduce an audio frequency oscillator per pixel at a unique frequency such that the beginning pixel at far left is given the lowest frequency in our range (say 200 hertz) on upward until the oscillator frequency at the far right pixel renders the highest frequency (say 10 khz) ... the grayscale value drives the volume of that pixel's oscillator

... further details at:  isomorphism between video and audio
                https://www.youtube.com/watch?v=DuiryHHTrjU

Beauty of this approach is it lends itself to performing this transformation in reverse (a bijection) - from audio to video we can use a Fourier analysis ( FFT ) of audio mapped into pixels - then back again to audio, rinse and repeat ...

Short answer
Yes, we can see with our ears.

Background
Bach-y-Rita famously stated "We see with our brains, not our eyes". Bach-y-Rita worked for decades on sensory substitution. Sensory substitution approaches in general aim to replace for a lost sense by redirecting information normally captured by that sense to another still functional one.

Bach-y-Rita focused on substituting vision by tactile information. His Tactile Vision Substitution System (TVSS) captured camera images and translated them to tactile images projected onto the back of blind subjects. His decades of research eventually culminated in the commercially available BrainPort device (Stronks, 2016).

Vision-to-auditory substitution devices have also been developed, most notably the vOICe by Peter Meijer and the prosthesis-substituting-vision-by-audition (PSVA) device, among others. The vOICe translates images into sounds by re-mapping their x-axis into the time domain, and their y-axis into the frequency domain (Meijer, 1992). This “image-sweepline” technique has subsequently been deployed in the EyeMusic device for use in sensory substitution (Abboud et al., 2014). The PSVA makes use of a pixel-by-pixel acoustic frequency transformation,where vertical position is coded as pitch and horizontal position as binaural intensity and phase differences, and brightness into loudness (Capelle et al., 1998).

Peter Meijer refers to the vOICe as generating 'soundscapes', much like the approach you are describing. I seriously encourage you to contact him, he is a very nice guy and open to exchange.

Anyway, to come to your question - can we see with our ears? Yes we can. Several studies have indicated that sounds can successfully be used to perform visual tasks, including localization (De Volder et al., 1999), pattern recognition (Arno et al.,2001a, 2001b) and depth-perception (Renier and DeVolder, 2010).

Several studies have shown that the visually deprived brain is capable of re-routing auditory sensations into visual equivalents by re-routing this information to the de-afferented visual cortex in the blind (reviewed in, e.g., Poirier et al., 2007). This is referred to as cross-modal plasticity of the brain.

However, the learning curve is quite steep, in that a lot of practice is needed to obtain useful information from visual information coded through sound (Stronks et al, 2015). Further, what is probably the biggest issue in analyzing soundscapes is visual clutter. While the visual system is very well capable of filtering out image clutter and extract the useful information, soundscapes will inevitably turn every irrelevant object in the scene into a corresponding sound. Front-end visual processing techniques are likely to be key to turning an auditory visual substitution device into a practically feasible device for the blind, or the sighted for that matter.

The visual cortex is recruited for auditory tasks in the blind, but not in the sighted. However, I am inclined to believe it is practice, and not visual deprivation per se, that determines the performance with sensory substitution approaches in general (Stronks et al, 2015).

References
- Abboud et al., Rest Neurol Neurosci (2014); 32: 247–57
- Arno et al., Neuroimage (2001a); 13(4): 632–45
- Arno et al., App Cog Psych (2001b); 15(5): 509–19
- Capelle et al., IEEE Trans Biomed Eng (1998); 45(10): 1279 - 93
- De Volder et al., Brain Res (1999); 826(1): 128–34
- Meijer, IEEE Trans Biomed Eng (1992); 39: 112–21
- Poirier et al., Neurosci Biobehav Rev (2007); 31(7): 1064–70
- Renier and De Volder, J Integr Neurosci (2010); 4(4): 489
- Stronks et al., Brain Res (2015); 1624: 140–52
- Stronks et al., Expert Rev Med Dev (2016); 13(10): 919-31


Molecular weight of my 2-D gel I am a little confuse when I try to figure out the molecular weight of the marker on my gel. I used NuPage Novex 4-12% bis-tris gel and Mark12™ Unstained Standard as a marker. Could please someone help me to figure out the molecular weight of the marker on my gel? I find different images in internet and I am confuse.

This is what I think. Does it help? Let me know if you need more information.


How genetically similar are worker ants from the same colony? I've been reading https://en.wikipedia.org/wiki/Ant and it says

  If the egg is fertilised, the progeny will be female diploid; if not, it will be male haploid.

Since the males have only one set of chromosomes to pass on to the queen, all of their direct offspring (which can only be female) will contain all of their DNA. How similar is the DNA that the queen provides? Is there a high likelihood that there will be genetically identical individuals within a single colony, even if they were hatched at different times?

Relatedness of ants within a colony vary from species to species (as different species may use different mating systems) and from colony to colony. I will consider a basic (simplified) model of a honeybee colony and describe it a little bit to try to address your question.

Simplified Model of an ant colony

There is quite a lot of diversity in mating systems among ant lineages. See for example the amazing case described in Fournier et al. 2005 (which is quickly summarized at the end of this answer). I will assume a general and simplified model below.

In general, a queen can have several mates. The queen is storing the sperm of these males in her spermatheca. As you noted, the queen is diploid while the males are haploids. The queen will use the stored sperm for all of her life. Each egg that is fertilized will give rise to a worker. Although, a worker does not reproduce (in our simplified model), a worker is still considered a female for morphological reasons. At some point in the life of the colony, some larvea that could have become workers are fed with royal jelly and they will then develop into queen. These queens will fly away to mate with multiple males and make up a new colony. The queen also produce males. The males are haploids. The queen only uses her own gametes to make up a male.

Relatedness

In our simplified colony, a male has no father and has the same mother than any other male and any other worker. Two workers may or may not have the same father. Let's imagine to simplify the story that the queen mated with a single male so that all the workers have the same parents (they are sisters).

queen-worker: 1/2
worker-worker: 1/2

This relatedness decreases with the number of father. At the extreme when there are an infinite number of fathers, the relatedness between two workers drops down to 1/4.

queen-male: 1/2
male-male: 1
male-worker: 1/4

The calculation of relatedness is a little bit problematic when comparing individuals that differ in ploidy (queen - male comparison for example).

Consequences of these relatedness

The fact that the workers are more closely related to their sisters than to their brothers have been suggested to cause a queen-worker conflict for the sex-ratio. Indeed if workers are more closely related to their sisters than to their brothers we might think that they would tend to bias the sex-ratio of the colony toward more sisters to a degree that would not be optimal for the queen. The degree of relatedness between workers depends on the number of fathers. There more fathers there are, the lower is the relatedness among workers and the lower is the incentive to bias the sex-ratio. As a consequence, while the queen would wish a sex-ratio of 0.5, the workers will deviate this sex-ratio toward more workers with a strength that is decreasing with the number of father.

Personally, I have some trouble with these predictions (that I won't express here) but empirical evidences (Chapuisat et al. 1997; Passera et al. 2001) support that the sex-ratio differ depending on the number of fathers (and therefore on the worker - worker relatedness).


Does the mutation CCR5-delta 32 increase the genetic info? My understanding is that the mutation CCR5-delta 32 caused the CCR5 co-receptor to be of a different shape, resulting HIV virus to not be able to attach itself to it.

My question, this shape/mutation, is it a result of a more or less information in the genetic information of the person with the mutation as compared to one without it?

Whether or not a mutation changes the 'amount' (meaning the size of the genome) of genetic information present in an individual depends on the type of mutation and is independent on which gene is affected.

In general there are 3 types of mutations:

point mutation: this is the change of one base pair to another (e.g. A to C). The total amount of information/the size of the genome is unchanged.
deletion: this means that a certain stretch of DNA is missing, likely disrupting what was there before. The total amount of information/the size of the genome is reduced.
insertion: this means additional DNA was added at a certain place in the DNA and probably disrupts something that was there before. The total amount of information/the size of the genome is increased.

The CCR5-delta32 mutation is caused by the deletion of a few (only 32) base pairs, however this deletion causes a frame shift in the gene and therefore leads to an early stop codon, which renders the protein inactive.


Fever vs Inflammation What's the difference between inflammation and fever? And why is fever called an inflammatory response? Does the word inflammation have both a general and a specific meaning?

Inflammation includes accumulation of inflammatory cells, such as neutrophils or macrophags, in a tissue. The typical four local signs of inflammation include redness (Latin rubor), heat (calor), swelling (tumor), and pain (dolor) (Britannica).

Fever is a symptom, which may or may not be present in a certain inflammatory condition. For example, lung inflammation in pneumonia is usually accompanied with fever, while joint inflammation in rheumatoid arthritis is not.


What insect is this? (Central Africa) I live in Africa (DR Congo). Here we have these insects that look like ants. They appear between May and June.

These insects give severe damage if crushed on the skin. They contain something like acid that burns the skin. I saw many people wounded by them.

So I would like to know what these insects are, and whether they can cause death if swallowed? Can someone point me to where I could learn more about them?

PS: There are no forests near where I live.

Edit:

The insects appear at the end of the rain season (April, May)  and right before the dry season (May, June).
Attracted by (neon) light. I think they fly only once then drop their wings (not really sure).
Can be found in homes (houses).
Can burn skin like acid.
It measures approximately 5 - 8 millimeters (not sure. can't find one right now).
Crawls fast with its tail upwards (don't know how to describe else, see image).
Solitary animal.

It is a Rove beetle of the Genus Paederus.

Why Paederus sp.?

They are brightly colored  rove beetles, Coleopterans with short elytra.
Have metallic blue or green-coloured elytra.
Have bright orange or red on the pronotum and basal segments of the abdomen.

There are widely spread on the planet and I found two species of Paederus sp. that are found in East of Africa, together they are called Nairobi flies.

The medical condition it causes is called Paederus dermatitis.

  According to Medical and Veterinary Entomology (2009) "At least 20 of the more than 600 species of Paederus beetles have been associated with Paederus dermatitis", even though Paederus beetles do not bite or sting.

  This skin irritation results from contact with pederin, a vesicant toxin in the hemolymph of many but not all females in the genus Paederus.

  The toxin is manufactured, not by the beetles themselves, but by endosymbiont bacteria, probably some species of Pseudomonas.

  Three different genera of rove beetles, all members of the same subtribe Paederina, can cause paederus dermatitis: Paederus, Paederidus, and Megalopaederus.

Pederin

  Pederin blocks mitosis at levels as low as 1 ng/ml, by inhibiting protein and DNA synthesis without affecting RNA synthesis, prevents cell division...

This makes it also a potent antitumour agent.

  The manufacture of pederin is largely confined to adult female beetles—larvae and males only store pederin acquired maternally (i.e., through eggs) or by ingestion.

  It is a contender of the title of most powerful animal toxin.

  It is among the most potent animal products known, more so than Latrodectus venom, which is 15 times more potent than cobra venom.

  Ingestion can cause severe internal damage and intravenous injection causes death ...

Further Reading:

1. Dermatitis Paederus: About 06 cases occurred in Bun
ia,
Democratic Republic of Congo

2. STUDIES ON THE MECHANISM OF ACTION OF PEDERINE, 1968

References:

 1. Paederus

2. Pederin

3. Paederus dermatitis

4. Encyclopedia of Entomology

5. The Role of Natural Products in Drug Discovery

6. ChEBI

Note: I found the picture in your question is the same as that of Wikipedia's picture of Paederus.


What causes tissues manifest the various forms that they do? A heart (or any other organ) is comprised of a group of cells. To the best of my knowledge, the growth of a heart depends on cell division. However, cell division by itself doesn't seem to explain why heart cells collectively manifest the form of a heart.

What causes tissues to manifest the various forms that they do?

This is a subject of active research. All the cells in the zygote are identical up to 8 cell stage. At the next division resulting in 16 cells formation it is called a morula.
The zygote has totipotent cells meaning each cell has the ability to develop into full organism by itself if it separates from the zygote (this is how identical twins are born).
Human zygotes are totipotent till at least 4 cell stage. In other primates experiments have demonstrated totipotency upto 16 cell stage.
The totipotent cells differentiate into pluripotent cells and then into various distinct cells belonging to different systems. This process is very complex and a lot of embryological factors and chemicals come into play.
The embryonic factors cause migration (called embryotaxis) and differentiation of the embryonic cells. Some of the factors are sonic hedgehog, wnt, insulin like growth factors, Hox, etc...
Different factors cause differentiation into different cell lines. These factors also cause the organs to attain specific shape and structure, thus the heart is shaped as a heart and the liver is shaped as a liver and so on.
Once the cells differentiate into a particular line, the stem cells of that region generally differentiate into that particular line due to the paracrine influence in that locus, even though these stem cells can differentiate into other cell lines when appropriately stimulated (thus demonstrating pluripotency). So intestinal stem cells would differentiate into goblet cells, surface epithelial cells, Enterochromaffin cells, etc... which are present in that locus.

For more see here:

http://www.sciencedirect.com/science/article/pii/S009286740800216X
http://www.embryology.ch/anglais/iperiodembry/controle01.html
https://www.bio.cmu.edu/labs/ettensohn/pdfs/dvg22746-2.pdf


Can someone identify this stinging plant? I have no idea where this plant came from, or what it is. What I do know is its leaves are covered in little hairs, there's little thorns growing all over it, and just by rubbing its leaf it burns you and leaves a red mark as well as blisters. It stung my mother and I would like to know what it is so I can find a remedy.

larger image:

http://i1094.photobucket.com/albums/i449/cupcaketurtle1/20150714_225505_zpskr24gklq.jpg

I think it is a common stinging nettle, Urtica dioica. It is a native to Europe, Asia, northern Africa, and western North America and is the best-known member of the nettle genus Urtica. As commented by others, your geographical location would be helpful to obtain a more accurate identification.

Like other stinging nettles, it is unpleasant to the touch, but harmless. Just be patient. The redness and burning/itching will disappear. If the pain gets serious or other complaints arise, go to your GP.

Stinging nettle. Source: Health Direct.


What "emotions" can a snake feel? Short:
Thinking in particular of a Royal Python (US: Ball Python) such as some people keep as exotic companion animals, what sorts of "emotions" or "feelings" are they capable of?

Long: http://simonsnakesite.tripod.com/snakebasics.html says that

  scientific studies show that snakes just don't have the cerebral capacity for [emotions like joy, anger, and affection] but do have "primitive" feelings like aggression, fear, and pleasure

Based on the parts of the human brain where we develop emotions, and on the more primitive brain in a snake, this makes sense, but beyond being able to tell whether it's feeling the primitives such as "fear" or "safety", what "emotions" or "feelings" can we realistically ascribe to a snake?

We can only very indirectly and tentatively ascribe emotions/feelings to animals if we understand their brains functionally, and use functional imaging. This is difficult in practice. There is also a crucial difference in science between the subjective world (happy) and objective world (smiling).

In ethology, you can only observe behavior and its consequences. Stimuli can be appetitive and aversive, positive or negative. Insects, reptiles and mammals can similarly differentiate between sweet water (which they seek out) and bitter water (which they normally avoid). Those are easier behaviors to identify. Of course, in reality, an emotional state is made up of a complex multi-dimensional spectrum of multiple measures (satiety vs. hunger, anxiety vs. relaxation, happiness vs. unhappiness, fear vs. safety, sadness vs. unsadness, etc.) simultaneously. There is also a difference between the measurement and the internal reality. Additionally, there's the choice of measurement and the internal reality, too. One could measure happiness by width of your smile at a given time, but that would not be a very valid and reliable measurement. This is the general difficulty with measuring and detecting emotion - behavior is a more objective quantification.

If you were studying a new species of human, which could not talk or report to you using a language about how it 'felt', and had a brain significantly different from ours, we would also be unwise to ascribe specific emotions so callously. Not because the specimen would be incapable of feeling emotions, but because we wouldn't have the tools to check and verify internal emotional states, or probe whether the snake was conscious of an emotion regardless of its behavior.

However, we do believe that emotions require a big central nervous system to exist. Snakes certainly have large enough brains to experience fear and pleasure. It seems that most large vertebrates can, certainly mammals can such as mice. Whether reptiles or even insects have the 'cerebral capacity' for non-primitive (read: non-humanlike) is an open question.


Do animals exist which have good vision, but see only grayscale? In computer vision the color information is often discarded, as most object recognition tasks seem to work just as well on the greyscale image (even better, because there is less unnecessary information).

Do animals exist which have good vision (e.g. see sharp, many details), but only see greyscale / very limited colors?

Preamble & Overview.
This is a rather unsatisfying answer I'm afraid. I can't seem to find any animal that has exceptional eyesight and sees in monochrome.
Baring in mind the context of humans vs machines; machines cope better with shapes rather than colours however it generally appears that those animals which rely on exceptional eyesight to survive tend to see in colour and have other neurological systems to ease "data overload".
Animals that see in grey-scale.
Some pinnipeds (seals) see in grey-scale, but note that their survival doesn't seem to depend on visibility, and it is generally regarded as poor even in a typically healthy animal. According to SeaWorld, researchers have found blind seal mothers and pups that are otherwise perfectly healthy.
Dolphins are a similar story. It is so murky that they rely on bio-sonar. Fresh water dolphins are almost completely blind.
In fact, the more species that I have read about which have monochromatic vision, the more I see that these animals rely heavily on other senses.
Some land animals with "decent" monochromatic vision:

Lorisiformes
Bats
Raccoons
Nocturnal kinkajous

Note that these often have another much more acute sense like smell or hearing.
Surprisingly, there is also not necessarily a link between monochromatic vision and nocturnal state (there are some animals with dichromatic vision that are nocturnal, and some animals with monochromatic vision are crepuscular, or diurnal and visa versa).
From wiki:

Many species, such as all marine mammals, the owl monkey, and the Australian sea lion have monochromatic vision under normal conditions...

A trend I see is that animals that have exceptional eyesight tend to have also evolved some sort of colour differentiation.
Why not ditch the colour info to make it easier on the brain?
To bring this back to your context of machines I would say that identifying the difference between a ball, a chair, a human, and a car (the sort of things machines need to know about!) is much more dependent on shape than colour. A monochromatic person wouldn't struggle with that at all.
However in a "wild" environment telling the difference between grass and tiger stripes means that an animal with trichromatic vision may get to live another day whereas the animal with monochromatic vision might not see the tiger in time. Or spotting berries and fruit in some distant trees might mean food that would have otherwise gone unnoticed.
Those are obviously very narrow examples, but generally it seems animals always have one or more exceptional senses limited to smell, hearing, or colour vision (it would be great if someone could point out an exception to this in the comments, like touch or taste!).
You are right to hint that there is a lot of information in colour vision. Like your example with loss of colour in machines, data needs to be dumped very quickly in the human brain.
I'm not a neuroscientist, but I have read pop articles about how little we can remember with photo detail. Within seconds of looking at a scene all texture details are lost, most objects are forgotten about and all we can really recall are big shapes. But importantly, we would notice the tiger in the woods before forgetting and run for it! If we had no colour input, that wouldn't be the case.

Examples of more colour being used.
Hopefully the above demonstrates that colours are important to many animals. If anything it seems that more colours even than our perception of the EM spectrum are preferable, particularly into the UV range.
For prey identification reindeer rely on ultraviolet light to spot lichens that they eat. This same sight can spot the UV-absorbent urine of predators. This article has a few more examples.
Some birds of paradise like parrots have even more brilliant patters under UV light. Even starlings look to have an identifying pattern under UV light. Both those examples are thought to be involved in mate selection.

White light does not reveal the feathers' yellow fluorescence in images (left), but short wavelength illumination does (right). Photo: Science

This all hammers home that colour is more important to animals than machines and is involved in more than just camouflage.


Are there any trees that prefer to grow on the floor of water bodies but protrude to the air? Are there any trees that prefer to grow on the floor of water bodies but protrude to the air? Specifically, those that prefer salt water or grow on shallow sea.

Mangrove swamp trees and shrubs immediately spring to mind. There are many species that fall into this category of trees that grow in intertidal and costal locations. They prefer locations where salt and freshwater mix, known as 'brackish water'.

All roots require oxygen and the species that fall into this category have developed roots that protrude above the surface, called pneumatophores.

Photo from http://www.dutchpickle.com/philippines/palawan/sabang-mangrove-forest-palawan.html

Here is an excellent website with more information
http://www.fao.org/docrep/010/ai387e/AI387E06.htm


How does an amoeba move? Simple question. It forms a pseudopod, and then flows in to it. But how does it move its material to form a pseudopod? And even so, if it is floating in water, what is it pushing against so that part of it holds still and part can move forward? It would be like trying to move while wearing ice skates by pushing your arms forward in the air: no net force is transferred.

It has a cytoskeleton, a network of fibers stretched across the cell which it can shorten and expand (by adding or subtracting actin monomers which build them) in a coordinated manner to more-less arbitrary change shape.

According to this paper, on surfaces they generally can adhere to it using membrane protein structures, thus the locomotion occurs due to friction.

To swim, they generate bumps near the front end of the cell and move them towards the back, similarly to how a swimmer uses hands.


How the conjunctivitis virus spread just by seeing a person's eye who is infected Conjunctivitis or 'pink eye'.

I have a few questions on conjunctivitis. When I was suffering from conjunctivitis, my doctor advised me to wear sunglasses so that no one else gets infected.

I wonder how it happens that if someone looks into an infected eye, then there is a chance for that person to also get infected. Specifically, why does this apparently happen only when we see an infected eye?.

Another question I have is why does our eye get watery when we see the eyes of an infected person?.

You can't catch conjunctivitis by looking at someone, but you can spread it around by touching your eye and touching something else, which then can pass the virus to someone else (viral conjunctivitis can be highly contagious). There are no hard facts, but one estimate is that people touch their faces an average of 3.6 times per hour, more if your eyes are itchy. Wearing sunglasses can not only help the possibly increased sensitivity of eyes with conjunctivitis, but they may also cut down on the number of times you touch your eye (thus spreading the virus).

There is no evidence to support that our eye get watery when we see the eyes of an infected person.

Conjunctivitis (Pink Eye) - CDC
Stop Touching Yourself, Flu Researchers Say


Are there any enzymes in cytoplasm to help the newly-synthesized polypeptide to form tertiary structure? Polypeptides made by ribosomes which attach to rER will go into the rER to form the tertiary structure. Those polypeptides made by free ribosomes usually stay in cytoplasm. So are there any enzymes in cytoplasm to help them to form tertiary structure?

There are several types of proteins that do this, all of which fall under the category of molecular chaperones. In particular, chaperonins such as GroEL/GroES complex in E. coli, sequester newly-formed polypeptides to allow them to fold their tertiary structure and avoid aggregation. Another widely studied class of these proteins are heat shock proteins (Hsps): these are involved generally in acclimating cells to stresses (such as heat), and some of these Hsps have been specifically implicated as chaperones. I'm a new user, so I can't post a 3rd link, but just google Heat shock proteins and you'll find plenty of information.


Why the length of UTR in the genomic sequence of gene X is too much longer than the same region in the corresponding Refseq mRNA sequences? I'm browsing in the UCSC genome browser and found that the UTRs length of KIAA0040
gene in the genomic sequences is too much longer than the corresponding the Refseq mRNA sequence. In fact, the total length of Refseq mRNA sequence is 4,721 and the length of its genomic sequence is about 36,107bp, of which the length of CDS is just 300 bp. How to explain this event?
This gene has 4 transcript variant and I know something about that UTR can span multiple exons, but I'm not sure about it and would like to hear more from you.

UTRs are involved in post-transcriptional regulation. See the wikipedia articles on the 5' and 3' UTRs. Alternative splicing of UTRs allows for exposing/hiding these regulation sites, which may then be useful for differential regulation in differing tissues.


What is the reason for 'microcytic' anaemia? I know the causes for microcytic anaemia are Fe deficiency, prolonged inflammation, Thalessemia, Sideroblastic etc. All these logically point to a decrease in Haemoglobin synthesis - either Haeme or globin.

But my doubt is, what exactly causes the microcytosis? Lesser Hb can explain the hypochromicity, but how does it explain the decreased MCV?

The reduced iron availability affects the red cell size during differentiation.

  The presence of red cells with reduced mean corpuscular volume (MCV) reflects reduced hemoglobin synthesis, which can have several causes. It can result from defects either in iron acquisition or availability, or in heme or globin synthesis. Experimental data in mouse demonstrated that early mitotic divisions are accompanied with no reduction of MCV, whereas during differentiation mitotic events are associated with a substantial reduction of MCV[1]

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2649346/

Coopersmith A, Ingram M. Red cell volumes and erythropoiesis. II. Age: density: volume relationships of macrocytes. Am J Physiol. 1969;216:473–82.


Why glycoproteins are better than non-glycoproteins in fulfilling biological tasks? I have just an intuition that the carbohydrate part of glycoproteins help them to fulfil those tasks like in plasma membranes.
You can also get many more receptors if you can use carbohydrates too.

For instance, glycoproteins are necessary in recognising white blood cells. Antibodies are examples of glycoproteins. So they play a crucial role in our innate and adaptive immunity: MHC interaction with T cells in adaptive immunity.
Other examples: necessary in platelet aggregation and adherence, components of zona pellucida and connective tissue. Some hormones are also glycoproteins so necessary in humoral adaptive immunity: FSH, LH, TSH and EPO.

But why glycoproteins are "better" than proteins without carbohydrates moiety in fulfilling biological tasks?

I still see that both are important, but why the one is better than the other one.

In other words: Are there any biological tasks that only non-glycoproteins can fulfil, not glycoproteins? Are non-glycoproteins necessary in some essential biological tasks?

I think the answer to the last two questions is "yes", so why would one say that glycoproteins are better in fulfilling biological tasks than non-glycoproteins.

The central reasoning is flawed because it places some intrinsic value on glycoprotein modification. The general intuition is that, if the protein is glycosylated, then it's likely for a reason, whether it be to help fulfil antigen recognition, adopt a correct conformation, or help in molecular tethering. Beyond, that, many (perhaps a majority) of cellular proteins are not glycosylated. Two important examples of cell membrane proteins that are not glycosylated would be endoproteases (eg, furin) and chemical transporters.


Do blood glucose "spikes" contribute to insulin resistance, or is prolonged elevation required? There's increasing public discussion about the health risks of chronic insulin resistance* (IR). In many cases there's a focus on high glycemic index foods that "spike" your blood sugar, which implies that a rapid increase in blood glucose is by itself sufficient to contribute to IR.

On the other hand, I've heard the claim that if a person is 1) moderately active, 2) not in caloric surplus, and 3) not already insulin resistant, then they will will quickly clear excess blood glucose by replenishing glycogen or through general energy expenditure. This is claimed to have no effect on IR, even though the individual was temporarily exposed to elevated glucose / insulin.

This leads me to two questions:

1) Is it true that high blood glucose is normalized substantially more rapidly in people who have depleted their glycogen, or who have higher energy needs?

2) Does repeated exposure to high levels of blood glucose contribute to IR by itself, or are high and prolonged levels of blood glucose required?

This has public health implications -- If the "spikes" theory is inaccurate, then glycemic index may not be very important to sufficiently active people**, and low glycemic index meals may not be as helpful as expected for people at risk of developing IR if total glucose exposure is high.

*"chronic insulin resistance" would exclude gestational diabetes and the reversible insulin resistance seen on ketogenic diets.

**For this discussion, let's ignore effects of blood sugar swings on hunger, mood, behavior, etc, since my interest is in the specific physiological triggers for IR.

Great Question.

The biggest problem is persistent insulin signaling from prolonged excessive high blood glucose over time. The reason being that it is this kind of signaling that results in insulin insensitivity due to down-regulation of the insulin receptors.

Any bolus of carbohydrates > ~ 25grams in a sitting is going to bump up blood sugar at a fast enough rate to warrant the release of insulin to help lower blood sugar levels.  This can be mitigated by an excessive amount of fat along with the carbohydrates, thus slowing down the spike.

  Your question: 1) Is it true that high blood glucose is normalized substantially more rapidly in people who have depleted their glycogen, or who have higher energy needs?

So this is a little confounded by several variables.  The thought process is that people that have less glycogen or higher energy needs, don't have insulin insensitivity; thus the same amount of insulin would do a better job of shuttling glucose into cells.  We know that consistent exercise increases insulin sensitivity, as does lack of persistent insulin signaling (such as comes from being in a glycogen depleted state).  So the answer to your question is generally YES for these reasons.

  2) Does repeated exposure to high levels of blood glucose contribute to IR by itself, or are high and prolonged levels of blood glucose required?

What we know from epi studies suggests that it isn't insulin spikes.  It is prolonged insulin signaling that causes insulin insensitivity through down-regulation of insulin receptors.

If you are fuel deprived, or only getting what you need from your food, insulin spikes are normal and transient and don't cause this IR.

Persistent insulin signaling causes many many side effects. Insulin is mitogenic,  has downstream pro-inflammatory cascades, and the insulin insensitivity that results is a major player in non-alchololic fatty liver disease.

Some references for these thoughts and further reading:

This one gives evidence of reduced IR activity, not
downreglation
Insulin signaling and NAFLD
Exercise and Insulin Sensitivity


Where is sialic group in gangliosides that form ABO blood groups? A ganglioside is a molecule composed of a glycosphingolipid (ceramide and oligosaccharide) with one or more sialic acids (e.g. n-acetylneuraminic acid, NANA) linked on the sugar chain. (source: https://en.wikipedia.org/wiki/Ganglioside)

Gangliosides form ABO blood groups.

Do gangliosides always contain sialic acid? If true, then where is sialic acid in blood groups?

Structural formula of ganglioside GM1a:

Blood Group Antigens:

I suspect this is a product of differentialy expressed glycosyltransferases. Instead of adding a sialic acid, for example, if you're coding for Enzyme B which is an alpha 1-3-galactosyltransferase, you're going to add a Gal to the glycan chain forming B antigen, and so forth. Sialyltransferases can add sialic acid groups, but to the same structure it looks like there is competition between the glycosyltransferases to add sugar moieties that results in different structures getting produced from backbone structures. Source, pages 5-10

  Type-1 units may be modified by glycosyltransferases that transfer sugars to either terminal galactose or subterminal GlcNAc, generating sialylated structures or blood group determinants. The synthesis of type-1 units and expression of the corresponding β1–3 galactosyltransferases are regulated in a tissue-specific manner...

Structures Common to Different Glycans

So that's to say there shouldn't be a sialic acid group on ABO antigens, though sialyltransferases are capable of forming Lewis Antigens (Source). In the anabolic pathway the backbone structure is simply getting attacked by glycosyltransferases and the pathway goes the direction whichever one wins out (level of protein vs level of substrate). Being said, I'm unsure it's proper to say ABO antigens are produced from gangliosides, but if anyone finds some faults in my explanation please let me know!

I'm looking into catabolic pathways that may produce ABO antigens by recycling gangliosides, probably resulting from some cleavages by other glycosyltransferases, I just haven't gotten there yet, I'll try to update if I find anything.


Has evolution made a mistake with prehistoric animals? Let me start this by saying I have very limited knowledge in biology and evolution.

However, when visiting museums and watching documentary movies, I always get impression dinosaurs (and other animals in "dinosaur era") are very huge compared to today's animals, especially land animals.

So I wonder, was the this huge size actually an error in evolution?

There are two questions here.

Dinosaurs were larger because their basic anatomy is better at being large than mammals. Their spine is better braced (no lumbar region), their breathing mechanism scales better, and their hip structure is stronger. This is called a preadaptation, or when an organism or group of organisms just starts with a head start on a particular adaptation due to unrelated reasons. It is the same reason mammals are the only terrestrial vertebrates to have echolocation: they are the only group with advanced amplification equipment in the ear to give it a head start.
Any era has its giants. Today is the time of the largest whales, largest trees, largest frogs, and largest horse to ever exist. Size is often a decent advantage: it makes you more resistant to resource fluctuation, it's just not a good for surviving global mass extinction inducing bolide impacts.

Evolution has no foresight. Evolution often produces and locks in counterproductive adaptations in the long run; while an adaptation may be an advantage in the short term, it may lock the organism into a disadvantaged position in the long run.
Sexual displays are a classic example: some quirk in peacock brains meant early female peacocks really liked more flamboyant males, that drove peacocks to the point modern males are incredibly vulnerable to predators and can barely fly due to carrying around huge superfluous tails. Both males and females would be better off preferring/having something less detrimental, but a feedback loop has locked in that detrimental feature. Males without it can't find mates, and females who do not prefer large tails male offspring also can't find mates. The term for this is fisherian or runaway selection. As an another example of counterproductive selection, many organisms when no longer controlled by predators or other factors will expand their numbers and consume resources to the point their populations collapse because there are too few resources to sustain them. Parasites often face this: a host with too many parasites dies, which is bad for the parasites but if the host can't fight off the parasites many are perfectly happy to kill their host and then starve.

Another aspect of evolution not having foresight is it cannot prepare you for extremely rare events, like mountains falling from the sky.


What does it mean to "nucleate multi-protein complexes"? I am reading an article about the mTOR signalling pathway and I have come across the following:

mTOR nucleates at least two distinct multi-protein complexes, mTOR
complex 1 (mTORC1) and mTOR complex 2 (mTORC2).

I am not sure what is meant by "mTOR nucleates 2 multi-protein complexes". From the paper, I understand that mTOR is a component of the mTORC1 and mTORC2 complexes. I have read the definition of 'nucleate' online and it means to either "to form into a cluster" or "to act as a nucleus for". However in the context of this article, I am not clear about what is meant by "nucleates" in the above statement. Any insights are appreciated.

Here nucleation has a rather physical meaning. mTOR acts as the starting assembly point of the complex.


CRISPR/Cas9: What are the main differences between sgRNA and the Cr:TracrRNA ? So from what I understand, in gene editing, the CRISPR vector expresses a small RNA sequence comprised of a small guide-RNA that is complementary to your target sequence. The sgRNA comprises a 20 Bp CrRNA and a truncated (cut down) TracrRNA right ?

My main question is how does this truncation enable gene editing ? After all, the bacteria have a full TracrRNA and not a truncated one.

You are correct about the components of the sgRNA.
However the truncation of the tracrRNA does not enable gene editing. Rather it is all that is required.
In bacteria the crRNA and tracrRNA are distinct molecules which must pair through the complementary palindromic repeat sequences. This is not the case in gene-editing as the crRNA and tracrRNA have been fused with a synthetic stem loop. Thus the palindromic repeat sequence is not required and the tracrRNA is shorter.
Check out Cong et al. (2013) in Science.


What causes the tonotopic organization of the inner ear? I'm trying to understand why tones are registered in the way that they are in the inner ear, i.e., why are high pitched sounds sensed at the base of the cochlea and low frequencies in the apex? I've been unable to find out the specifics of this tonotopy, but as far as I can gather this is due to the physical properties of the basilar membrane.

But what exactly are those physical properties? Does the basilar membrane vary in size and stiffness along its length, so that each bit has its own resonant frequency, or is there something else going on?

The frequency tuning in the cochlea is due to a number of factors.

The primary factors of cochlear frequency tuning are generally ascribed to the passive physical characteristics of the basilar membrane (BM), which OP already identified in the question - The BM is wider and more flexible at the apical end (low-frequency region) and narrower and stiffer at the basal end (high-frequency region). Like the strings on a guitar, stiff and thin cords produce high-pitched sounds, while loose and thick cords produce low-frequency sounds. The stiffness of the BM gradually decreases from base to apex, while its width gradually increases along that length, thereby creating the gradient of characteristic frequencies of the basilar membrane (Purves et al., 2001) (Fig. 1).
Another factor that may play a role is the length of the stereocilia. Stereocilia are the mechanotransductive hairs that give the hair cells their name. In the inner hair cells (IHCs) the stereocilia are mechanically deflected when a sound wave eneters the cochlea. That in turn leads to neurotransmitter release from the IHC and that in turn stimulates the auditory nerve. The stereocilia increase in length towards the base of the cochlea. Longer stereocilia respond most optimally to longer wavelengths (lower frequencies). Hence, stereocilia length also provides another mechanical gradient that facilitates frequency decomposition in the cochlea (Snow & Wyckam, 2009).
A last factor is more physiological in nature; the frequency tuning of the cochlea is much sharper than can be explained on the basis of the passive membrane properties of the BM. For example, studies in dead cochleas show a shallow tuning of the BM, while the tuning in alive cochleas is much sharper. Hence, it is thought that an active mechanism has to be at play. Generally, the outer hair cells (OHCs) are attributed this function. OHCs start to increase and decrease in length when the BM moves in response to sound. They are thought to amplify the BM response to sound. If these OHCs only amplify a very narrow set of frequencies and not others, they may indeed be capable of sharpening the tuning curve of the associated nerve fibers, but the exact mechanism behind this is unknown (Purves et al., 2001).

Fig. 1. Frequency tuning along the basilar membrane. source: Purves et al., 2001

References
- Purves et al. (eds.) Neuroscience 2nd ed. Sunderland (MA): Sinauer Associates (2001)
- Snow & Wyckam, Ballenger's Otorhinolaryngology: Head and Neck Surgery, John Jacob Ballenger (2009)