The answer to your question in general is yes.
There are many salts and compounds that are endothermic - they cool the solution when they dissolve.  It also turns out that glucose is endothermic when it dissolves if this sheet i found is to be believed.  Its not a strong effect but you made an accurate observation!

Endothermic salts can be quite cold.  This is how home ice cream makers often work in fact - rock salt dissolves into the ice and makes it even colder than it started out to be. I believe that is how ice cream was made before refrigeration and ice storage arrived in the 19th century.


Why are there no organisms with metal body parts, like weapons, bones, and armour? (Or are there?)

There are some cases, as hinted at by the comments. But these are relatively small amount of metal.

Its not that there is no metal available, but I can think of several reasons you don't see iron exoskeletons on animals all the time.  Firstly, fully reduced (oxidation state 0) metal has a high energetic cost to create in reduced form.

Iron is the second most common metal after aluminum on the earth's crust but its almost entirely present in oxidized states - that's to say: as rust.  Most biological iron functions in the +2/+3 oxidation state, which is rust or closer to it than metal.  Cytochromes and haemoglobin are examples of how iron is more valuable as a chemically active biological agent than a structural agent, using oxidized iron ions as they do. Aluminium, the most common metal on earth has relatively little biological activity one might assume because its redox costs are even higher than iron.

If there are some reasons why reduced biometal doesn't show up very often, inability of biological systems to deposit reduced (metallic) metals is not one of them.  Bone and shell are examples of biomineralization where the proteins depositing the calcium carbonate or other oxides in the material are structured by the proteins to be stronger than they would be as a simple crystal.  There are cases of admittedly small pieces of reduced metal being produced by biological systems. The Magnetosomes in magnetotactic bacteria are mentioned, but there are also cases of reduced gold being accumulated by microorganisms.

I would say that while iron skeletons might seem to be an advantage, they are electrochemically unstable - oxygen and water will tend to oxidize (rust) them quickly and the organism would have to spend a lot of energy keeping it in working form.  Electrical conductivity sounds useful, but the nervous system favors exquisite levels of control over bulk current flow, even in cases like electric eels, whose current is produced by gradients from acetylcholine.

What's more, it is a fact that biological materials actually perform as well as or better than metal when they need to.  Spider silk has a greater tensile strength than steel (along the direction of the thread). Mollusc shells are models for tank armor - they are remarkably resistant to puncture and breakage.  The time it would take for metalized structures to evolve biologically might be too long - by the time the metalized version of an organ or skeleton got started, the bones, shells and fibers we know probably have a big lead and selective advantage.


Are Asian people genetically predisposed to be shorter than Europeans?

Note: This is too long for a comment, so I will post it as an answer, even though it is merely an example and not a full answer to your question.

An example of the environmental influence on human body height can be found in the statistics assembled by the Swedish conscription service from 1840s to 2010 (when general conscription ended). During this time the average height of Swedish men (aged between 18-21) increased from 167.4 cm (in 1841-45) to 180.2 (in 2004), an increase of 12.8 cm or 7.6% (Werner 2008, unfortunately in Swedish, but tables 2 and 3 should be understandable). Here is a graph of the data found in the paper:

During this time Sweden has gone from what would have been a bottom-20 position in the wikipedia list of average human heights (close to contemporary India or Mexico) to a top-10 position. This is clearly not due to changes in the genetics of the population, but to changes in the environment (probably mainly due to nutrition). I know that many countries have gone through a similar development, and this is usually refered to as a secular change or trend in body height and weight (see e.g. Roche, 1979 and Loesch et al., 2000 for further examples).

Nothing of this naturally contradicts that genetics is a powerful determinant of human height. However, it shows that the average height in two countries cannot be compared in a meaningful way (at least if you want to infer genetic differences) without knowing something about the nutrition status and the average living conditions in both countries. The situation is rather that genetics is setting the limits of potential height, but that environmental factors will determine the actual outcome. This is also discussed in the paper above, but there are certainly better references to be found in English. In the reference list (#9, #10) you can also find examples of how there are also well-known genetic determinants of e.g. short stature in some human populations (in this case decreased insulin-like growth factor I receptor expression and function in African Pygmys, see ref #10)


What is the purpose of the AraC gene in pGLO?

The AraC gene can activate GFP expression, because the GFP in the pGLO plasmid has the negative inducible pBAD promoter:
In the absence of arabinose an AraC protein dimer binds the promotor region, but does not activate transcription. When arabinose is present, the protein binds in a different way, which allows the downstearm gene (here GFP) to be produced.

According to this plasmid map I found the AraC and GFP genes are in different orientations (and facing 'away' from each other), so transcription of AraC wouldn't run over into GFP even without a terminator present.


Why are 3 nucleotides used as codons for amino-acid mapping in DNA?

The central dogma of molecular biology: DNA makes RNA makes Protein

DNA is a reference for proteins*, which are the functional molecules in cells. These are comprised of 20 unique amino acids, and each is coded for by a stretch of DNA known as a codon. Codons are always 3 base-pairs (nucleotides) in length.

DNA is made of 4 unique nucleotides; (A)denine, (G)uanine, (C)ytosine and (T)hymine. This means that there are 64 unique codons that can be made with these 4 bases (4*4*4).

Theory One - evolvability

If codons were only 2 bases in length then the variety of codons that could be created would be less (only 16 unique sequences if there are still 4 nucleotides). More unique nucleotides would be required to get enough unique sequences to code for the 20 amino acids (as well as the STOP codons). For instance, to get 64 unique sequences using a 2-bases-per-codon system there would need to be 8 unique nucleotides.

We cannot ever 'know' what happened in evolutionary terms, but it seems likely that the 3-base (nucleotide) codon system would have arisen after a period of a 2-base system, as the biological systems became more complex. This would have allowed a lot more variation in the amino-acids used, and thus more "evolvability", which would have been very advantageous to early organisms.

However as the 4-unique-nucleotide/3-codon system is ubiquitous to all life we have discovered on earth, it seems likely that, back at the start of DNA (in fact probably RNA), this was the system that worked, or at least, this is the one that survived (although as Kevin rightly points out, we don't know whether there ever were any other systems). Variations may have arisen over the years, but it is this 1 system that has prevailed here on Earth.

See this question for some more interesting info: why-20-amino-acids-instead-of-64?

Theory Two - "redundancy" of codons conveys additional information

This theory is not mutually exclusive to the one described above. In a recent paper D'Onofrio and Abel [1] state that ribosomes pause for different lengths of time at different codons (even if the codon codes for the same amino acid), and that this pausing affects the 3-dimensional structure of the final protein.

Therefore the nucleotide sequence contains at least two "layers" of information: firstly which amino-acid should be added, and second the specific codon used for that amino acid can impact on the final structure of the protein. This could not be done with fewer nucleotides, but arguably even more control could be exerted with more nucleotides, but perhaps this comes back to my first point that this system evolved such a long time ago that more nucleotides were not necessary for life to "work" and proliferate into everything we see today.

D'Onofrio and Abel, 2014. Frontiers in Genetics. Redundancy of the genetic code enables translational pausing

*only around 1% of our genome is actually protein-coding, and many non-protein-coding RNA products have very important functions, but I won't go into this here. Suffice it to say I am referring to the protein-coding regions of the DNA.


How do I tell if the mosquitos in my New York City apartment can carry Zika?

This is a reasonable question, and I was surprised to find that official information on whether Aedes aegypti is present in NYC isn't very clear. I personally would have thought that NYC was quite far beyond the range of Aedes aegypti (the 'yellow fever mosquito', believed to be the main vector of Zika virus in the ongoing emergence event in South America), and the New York City Department of Health apparently agrees with me:

  Aedes aegypti has not been found in New York City.

...(emphasis theirs) which seems pretty clear cut. However, the CDC recently published a map claiming that NYC is within the potential range of Aedes aegypti.

It's not really clear exactly what they mean by this. From the webpage:

  The new estimated range maps have been updated from a variety of published and unpublished sources.
  These maps show CDC’s best estimate of the potential range of Aedes aegypti and Aedes albopictus in the United States.
  These maps include areas where mosquitoes are or have been previously found.

A related species, Aedes albopictus, is sometimes found in NYC during the summer and is probably capable of transmitting the strain of zika virus currently circulating in the Americas (see for example this recently-published experimental infection study). Aedes albopictus has been the major vector in some previous zika outbreaks in other parts of the world.

(Edit (14th June): A group of mostly-CDC entomologists just published a map of locations where Aedes aegypti and Aedes albopictus have actually been collected between 1995 and 2016 here, and there's an NPR article explaining why the maps are different here).

Whether the density of this species or the temperatures are sufficient to sustain transmission for any length of time in a climate like that of NYC is a more complicated story. The CDC even adds:

  Maps are not meant to represent risk for spread of disease.

But you've asked whether the mosquitoes in question can carry zika, not whether they're likely to be good at it, so I'll leave it there. The short answer is that if they're Aedes mosquitoes, then they might be able to.

So how do you know if they're Aedes mosquitoes? Aedes are visually quite distinctive; they have black bodies with white stripy abdomen and legs:

(Image taken by Muhammad Mahdi Karim; details and license here).

Aedes are also generally day-biters, so if you're getting bitten at night that makes me suspect you've got something like Culex mosquitoes instead (which might be able to spread West Nile virus, although that's a different story). These are dull brown.

If you do find you have Aedes and you'd like to try to identify them to species level, you could collect some dead ones and look at their thorax. If you take some photos and post them here as a species-id question you'll probably get an answer pretty quickly, but this figure illustrates the difference between aegypti and albopictus:

(Image from WHO (1995) Guidelines for Dengue Surveillance and Mosquito Control, Second Edition)

There are better images here but I think these are under copyright.


An online tree of life with extinct species present?

The tree of life project is your best bet, its not 100% complete but it is more complete than any other project I have ever seen, and unlike most actually includes many if not most extinct taxa. http://tolweb.org/tree/phylogeny.html
It also includes citation and brief descriptions of links and groups to make it easier. Some extinct lineages suffer from unresolved phylogenies but many of those are in constant flux or are actually unresolved in the fine scale so I can't blame them, especially considering they were originally based entirely on genetics, and is updated constantly.


Do "scars" in humans replace all the skin layers or only some layers?

This depends on how deep was the initial wound, and how that wound healed. There are mainly two ways a wound could heal, either by primary intention (like in surgically closed wounds), or by secondary intention (like in wound left to scar up with the edges not closed properly).

In very well closed wounds that involves all layers of skin, such as primary intention healing following plastic surgery on previously healthy skin, the skin would regenerate all the layers after a long process that could last for 2 years or longer and involves constant life long remodelling of the remaining scar.

In wounds healed by secondary intention, such as following a third degree burn without treatment with skin grafts, there is extensive scaring (mainly consistent of collagen which could be thought of as a filler and adhesive that allows the epithelial skin layer only to grow over it, without renewing the deeper layers). In such cases the scar is large, adherent to underlying tissue, and has only a thin overlying layer of epithelial skin cells. This scar might also be insensate (numb) as a result of superficial nerve injury due to the initial wound.

Most scars are somewhere on the spectrum between the two extremes mentioned above. A badly sutured surgical wound, or a surgical wound that gets infected later, might still heal by secondary intention causing extensive scaring that doesn't replace all the skin layers. A good plastic surgeon might later remove that scar and allow the wound to heal by primary intension to improve the outcome.

If you would like to expand on how wounds heal, here are a couple of links to start you off:

http://teachmesurgery.com/skills/wounds/wound-healing/
https://emedicine.medscape.com/article/1298129-overview


That is a bagworm. Order Lepidoptera, family Psychidae. You can read about them here https://en.wikipedia.org/wiki/Bagworm_moth


Did birds descend from a single or multiple species of dinosaur?

The answer is "one common ancestor", but I'll expand.

All organisms descend from one common ancestor so that question is not quite well-posed, but what you are actually asking I think is whether birds all descend from one common ancestor that was a bird, or whether their common ancestor wasn't a bird, which implies that different branches of birds became birds independently. In other words, are birds a "polyphyletic" group or a "monophyletic/paraphyletic" one (the difference between the latter is whether all of that common ancestor's descendants are birds, or whether it also had descendants that aren't birds).

The answer to that is that modern birds are monophyletic: they all descend from a common ancestor that, itself, was a bird. (and that common ancestor doesn't have any descendants that aren't birds)

But modern birds aren't the whole story - their group originates in the Cretaceous, and there are many groups of birds that are clearly recognizable as birds but also aren't modern birds - they might have teeth, they have subtle but unavoidable skeletal differences, etc. Like Enantiornithes and Confuciusornis. In other words, modern birds absolutely, unambiguously have a common ancestor that was itself a bird, which isn't hard because animals we would recognize as "birds" were already common by the time it appeared and the ancestor of our modern birds was just one of them. Whether those older, "extended" groups of birds themselves descend from a single species is harder to tell because fossil evidence is all we're going on, and it's even harder to tell when we go closer to the origin of birds and they no longer look unambiguously like birds. But at that point it's not so much a matter of "did this group originate from one ancestor or several" but "are these fossils that we've been putting in this group as closely related as we were assuming?" and "did this trait that these different fossils have evolve in their common ancestor, or did they evolve it independently, and what about those other fossils that seem related but don't have the trait: did they lose it from the common ancestor who had it or are they a sign that the common ancestor didn't have it to begin with?". Like, you might get different answers depending on how you define "bird". BUT paleontologists these days like monophyletic groups, so whichever groups they call "bird", those will have a common ancestor that was a "bird".

The Wikipedia page for Avialae expresses some of the issues with what "bird", or "Aves" means in the context of paleontology. To quote:

  Aves can mean those advanced archosaurs with feathers (alternately Avifilopluma)
  Aves can mean those that fly (alternately Avialae)
  Aves can mean all reptiles closer to birds than to crocodiles (alternately Avemetatarsalia [=Panaves])
  Aves can mean the last common ancestor of all the currently living birds and all of its descendants (a "crown group"). (alternately Neornithes)

"Avialae" is one of those "extended groups of birds", in that paleontologists will often refer to any member of that group as "birds", but there's still a wide gap between "Avialae" and "Neornithes"; some stepping stones on that gap:

Neornithes (modern birds) are part of
Euornithes (birds have a certain articulation oriented like modern birds, as opposed to Enantiornithes, or "opposite-birds", who have it the other way, in addition to other differences like having teeth; note this page has a cladogram), which is one branch of:
Ornithothoraces (all descendants of the common ancestor of Euornithes and Enantiornithes), which is part of
Avebrevicauda ("short-tailed birds", to distinguish them from long-tailed Avialans like Archeopteryx) which is part of
Avialae, which as mentioned is basically birdinosaurs that could fly like Archeopteryx but it doesn't stop there because that's part of
Paraves, a group of dinosaurs that by and large had wings and feathers including the four-winged dinosaurs like Microraptor gui, which if we saw today we'd recognize as not like other birds but would we recognize as not a bird, really? That's part of
Pennaraptora, which is the first group to contain names that we definitely think of as not-birds; this group contains birds as well as Oviraptor and Deinonychus, but to quote the page:

  The earliest known definitive member of this clade is Anchiornis, from the late Jurassic period of China, about 160 million years ago.

And Anchiornis, as its name suggests, is bird-like, feathered wings and all. This is where we get into "wait, Velociraptors were basically like turkeys?" reactions (Deinonychus is Jurassic Park's "Velociraptors").

(also these points are where the groupings become disputed, or fast-changing, or ambiguous between groups that are defined based on phylogeny, or similarity, or others and you can get different results depending on which group's Wikipedia page you look at; for example the Wikipedia page for Theropods puts Avialae directly under Maniraptora).

Pennaraptora is part of Maniraptora, which also contains your velociraptors, and Maniraptora is part of Coelurosauria which also contains your Tyrannosaurs. At this point we have clear non-bird dinosaurs, although it's likely they all had feathers.

I don't know which articles you read saying some birds would have descended from T-Rex and others from Velociraptor; that seems completely counter to what we know today of bird evolution, even if we extend "birds" to "Avialae" or even "Paraves". In fact the only way it would work is if we call T-rex or velociraptor themselves "birds". What you could have is conflicting articles about how close birds are to T-rex or Velociraptor; that part of the family tree is based entirely on fossils and so new fossils can change our understanding of how things are related... But the current phylogeny that makes, say, Avialae a group that's quite a few nodes away from velociraptors, and both of those a couple of nodes away from T-rex, seems quite robust. We have found many, many bird and proto-bird fossils in the last few decades that have clarified the picture on that scale (you can get an idea of how many by clicking the various links).

One thing those many, many bird and proto-bird fossils also made clear is that the traits of modern birds (feathers, wings, toothless beaks, etc) didn't evolve in a simple line from non-bird to bird. Many of those traits evolved convergently in several lineages, were lost in some, maybe regained in others, and feathers in particular turn out to be a widespread dinosaur feature that cannot be considered a uniquely bird trait anymore (unless we want to call T-rexes "birds"). Still, saying "beaks evolved several times" or "feathers evolved several times" doesn't mean that birds, let alone modern birds, evolved from several different ancestors. It can mean that the common ancestor of birds had lots of variously bird-like more-or-less distant cousins living around the same time.


Where can I download a list of all plant species of the world?

This website claims to contain all the plant species we know of (and also contains some statistics on the state of their collection). Keep in mind that there are many species that have yet to be found or assessed correctly. The world is a big place.
http://www.theplantlist.org


Basically just search "thing you want" and "phylogeny" and you'll find a million results on Google.  For you, I might recommend the Botanist in the Kitchen blog, which has a whole page on the subject and has assembled this phylogeny, including many, many others.  It's pretty impressive!


What's the mechanism for being mentally tired?

There is ongoing research on this topic, but there is a theory known as inhibition theory. It has been defined as:

  Inhibition theory is based on the basic assumption that during the performance of any mental task requiring a minimum of mental effort, the subject actually goes through a series of alternating latent states of distraction (non-work 0) and attention (work 1) which cannot be observed and are completely imperceptible to the subject.

For a more in-depth explanation, see this paragraph from Wikipedia:

  Directed attention fatigue occurs when a particular part of the brain’s global inhibitory system is overworked due to the suppression of increasing numbers of stimuli. This temporary condition is not a clinical illness or a personality disorder. It is rather a temporary fatigue of the inhibitory mechanisms in the brain. According to inhibition theory, it is natural for one to alternate between periods of attention and distraction. Although one’s efforts may involve very different tasks, each incoming stimulus calls upon the same directed attention mechanism.

or this paragraph from NCBI:

  Recently, it has been shown that the neural mechanisms of mental fatigue related to cognitive task performance are more complex than previously thought and that mental fatigue is not caused only by impaired activity in task-related brain regions. There is accumulating evidence supporting the existence of mental facilitation and inhibition systems. These systems are involved in the neural mechanisms of mental fatigue, modulating the activity of task-related brain regions to regulate cognitive task performance.

In short, it is now believed that the brain contains mental facilitation and inhibition systems, which control mental freshness and fatigue. Basically, when you concentrate, you actually stop all distractions from taking over (and not give more focus to the main point). This mechanism is governed by the inhibitory system of the brain. After some time, this system stops working ('it gets tired') and you become unable to pay attention towards anything. That's  why it is advised that after some time of concentration, you need to distract yourself (to refresh your inhibitory system); like, say, while preparing for exams, you should have a break of 5-10 minutes after studying for about 45 minutes.

Now, why mental tiredness causes physical fatigue can be (I think) summarized by the diagram below from here:

The exact process at this part is rather very interesting. Here, the neurons are not firing as quickly as they do normally. See this Wikipedia page:

  Physical fatigue can be caused by a lack of energy in the muscle, by a decrease of the efficiency of the neuro-muscular junction or by a reduction of the drive originating from the central nervous system. The central component of fatigue is triggered by an increase of the level of serotonin in the central nervous system. During motor activity, serotonin released in synapses that contact motor neurons promotes muscle contraction. During high level of motor activity, the amount of serotonin released increases and a spillover occurs. Serotonin binds to extrasynaptic receptors located on the axon initial segment of motor neurons with the result that nerve impulse initiation and thereby muscle contraction are inhibited.

The same might happen in the case of mental fatigue i.e. the excess serotonin released from frontal or parietal lobes, or even the inhibition system itself, can cause the same effect i.e. inhibition of muscle contraction.

References:

Inhibition theory
Directed Attention Fatigue
Neural mechanisms of mental tiredness
Mechanism of physical fatigue from mental tiredness
Fatigue


Can all animals of the same species crossbreed?

Species definitions are a somewhat contentious part of biology. There are no hard boundaries in nature that mean "this group here is one species, this group here is another species". Some people don't even believe that species truly exist and there are only gradations of relatedness. That being said, the Biological Species Concept is one of the more popular species definitions.

From the linked website: "The biological species concept defines a species as members of populations that actually or potentially interbreed in nature". Thus, by definition, all animals of the same species can and do interbreed in nature. If two individuals breed in nature, they are considered the same species (under this definition).

Of course, you can already see some problems with this definition. Under the BSC, are a dog and a wolf the same species? Do dogs and wolves breed "in nature"? Of course, fertile half-dog half-wolf animals exist, but does it even make sense to ask whether a domestic species breeds "in nature". I suppose you can say they can "potentially" breed in nature. But how do you define "potentially" breeding? Asking questions about species can lead to many exciting debates.


What conditions should I use for Gel Red staining?

I have had success with 1.5% agarose gels in TBE pre-stained with gelred.  I use a 10,000x stock solution of gelred sold by http://biotium.com.  I visualize the gel on an old fotodyne UV transilluminator.

After melting agarose in the appropriate volume of TBE in a microwave, I let it cool to about 50 C (I can touch the flask with the back of my hand without snatching it away) and then add the appropriate volume of stock gelred.

For a 30 mL 1.5% agarose gel:

mix 0.45g agarose + 30 mL 1x TBE
microwave until agarose solution boils and clarifies
let cool to around 50 C
add 3 uL gelred
swirl the mixture
cast the gel (don't forget comb)

This typically works for me.  I run the gel in a 1x TBE buffer at around 120 volts.


Computational engineering of protein binding pocket

You can try an evolutionary algorithm. If you can quickly evaluate the binding affinity you can initialize a set of copies of your protein but with random mutations. You can assign them a fitness score based on the affinity of the binding. The ones with highest affinity you replicate again with some probability of mutating each amino acid and you continue for as many generations as you need. If you find your parameters (mutation rate, population size, etc) correctly you can easily optimize the binding without knowing anything a priori about the different sites. There is a lot of literature on this, I suggest you do a quick Google scholar search on directed evolution or evolutionary algorithms to optimize binding affinity.

Paper on in silico evolution to optimize protein-protein binding


Why will world population keep growing if all women have only 2.1 children

As you mention, the population-lag effect is responsible for this. From The Wikipedia article on TFR: http://en.wikipedia.org/wiki/Total_fertility_rate#Population-lag_effect

  A population that has recently dropped below replacement-level
  fertility will continue to grow, because the recent high fertility
  produced large numbers of young couples who would now be in their
  childbearing years.

Thus, even if the current TFR implies long-term stability, the recent history of TFR values will continue to affect birth rates, and thus population growth/decrease, in the future.

Imagine that you have a stable population, with static birth and death rates. Now imagine that the birth rate during a single year for some reason doubles before dropping back to normal the next year, thus transiently increasing TFR. Now, it is easy to see that when the newly born, larger-than-normal generation reaches reproductive age, the population will increase again because the birth rate will increase in proportion with the size of the generation, while the death rate is unaffected until the enlarged generation reaches old age and starts dying off. Later, the population will decrease to its long-term stable level, which will be larger than before the TFR spike.


This is probably a land planarian, a flatworm (Plathyhelminthes) from the Subfamily Bipaliinae, called "hammerhead worm". This Subfamily is native to the Indian subcontinent, which matchs your description.

According to Wikipedia,

  The subfamily Bipaliinae is characterized by having a semilunar head that gives them the common name "hammerhead worms". The head has peripheral sensory pits on the ventral side and small peripheral eyes on the dorsal side.

You can see this semilunar head on the animal's anterior end (right hand side in your photo).

This subfamily contains the largest flatworms known. The larger one is Bipalium kewense, which can grow up to 40 cm.

However, the individual in your photo doesn't seem like B. kewense, which is a quite narrow worm and has a large head, with a different colour and stripes pattern:

Source: https://niceworms.wikispaces.com/Bipalium+kewense?responseToken=05b65f9b09b41aa5da58c3026c7f3ce8e

The one in your photo seems more like B. adventitium, which is a bit wider and has a smaller head:

Source: https://www.inaturalist.org/taxa/82290-Bipalium-adventitium

The problem is that B. adventitious adults are only 10 cm long, and that is hardly humongous.

So, I'd just say "it is a Bipaliinae flatworm", without narrowing it down to the species.

PS: It's not a leech (Annelida) because, among other clues, it clearly lacks metamerism.


An hormone is not different from most other molecules. To have an effect on a cell it binds to a (more or less specific) receptor, located either on the plasma membrane or inside the cell, and it initiates an intracellular cascade of events1.

There are several ways an hormone can have different effects:

there can be multiple receptors for the same hormone. For instance, prolactin can bind to two receptors, called prolactin receptor (PRL-R) short and long form. The short form of the receptor has been shown to lack the ability to promote milk protein genes transcription (See Lesueur et al., PNAS - 1991).
the same receptor can be coupled to different intracellular pathways in different cell types / physiological conditions, thus resulting in different effects.
each cell type/tissue expresses a set of protein that will interact in a different manner with the intracellular cascade promoted by the hormone.
an hormone can interact with receptors for other molecules. For instance allopregnanolone, a metabolite of progesterone, is a potent agonist of the GABA-A receptor, giving it anxiolitic properties.

An interesting example is that of estrogenic compound. Several receptors exist for estradiol (E2). The "classical" receptors are called ER-alpha and ER-beta, and they are located in the cytoplasm. The binding of E2 to the ER promotes their dimerization and entrance into the nucleus where they can promote the transcription of various genes. ERs can also bind to other transcription factors and modulate their activity. So, depending on which transcription factors are present different genes will be transcribed in response to E2. Moreover, ER-beta can have opposite effects then ER-alpha (see for instance Weihua et al., PNAS - 2000). In addition, receptors like ERs can be activated also in absence of the endogenous hormone: for instance, dietary amino acids activate ER-alpha in liver by a mTOR-dependent phosphorylation (Della Torre et al., Cell Metabolism 2011)

To make things more complicated, membrane receptor for estrogen have been described, such as GPR30 (Revankar et al., Science - 2005), membrane "versions" of the classical ERs, plus various splicing variants of the ERs (mostly expressed in tumoral tissue).

GPR30 in breasts has been shown to activate certain molecular pathways (notably Erk1/2) that contribute to cellular growth (Filardo et al., Mol Endocrinol. - 2000), possibly linking it to proliferation of ER-negative breast tumours. Other tissues that do not express GPR30 will lack this E2-induced proliferative stimulus.

So, tissue- or time- dependent modulation of the receptors and of the intracellular pathways associated with it can allow the body to respond to the same hormone (or, more in general, to the same molecule) in opposite ways.

1 This is a simplification, not every substance (and not every hormone) acts by binding to receptors, but let's keep things simple.


The question is asking which is NOT true.  You are correct that C is true - very few cells should be found in anaphase or telophase.

D is also true.  When spindle fibres are dissolved, chromosomes/chromatin would not be tightly bundled or packed in the cell and it would be easier to see them with an acetoorcein stain.

A and B are trick answers.  In a regular tissue, most cells are in interphase at any given time.  Interphase is the regular functioning period for the cell.

However, the question is referring to onion root tips which are primarily comprised of actively dividing cells (meristem tissue). The colchicine would affect most cells and most cells would be found arrested in the metaphase.  http://w3.marietta.edu/~biol/introlab/Onion%20root%20mitosis.pdf

Therefore for onion root tips treated with colchicine, most cells are not found in interphase.  A is the correct answer.


Organisms using thermal energy as their sole energy source

I had to re-read your last sentence a few times to make sure I understood it correctly, but I think that now I do, and I can answer your question.

What you're talking about are thermophiles. They're small organisms that love hot conditions - up to nearly 250 degrees Fahrenheit. They can be found places with a lot of hot water, such as hot springs - and, yes, ocean vents. Many use sulfur as a fuel during chemosynthesis, oxidizing it to make sulfuric acid. They take the energy from the heat source to do this.

Not all thermophiles use chemosynthesis. Those in hot springs may get a lot of sunlight, and they can use photosynthesis. However, those in the deep sea cannot undergo photosynthesis, and are forced to use the energy from the vents to undergo chemosynthesis. In fact, entire ecosystems can be built off them!

Thermophiles may even have been some of the first organisms on Earth. Around the time that life is thought to have first formed, Earth wasn't a very hospitable place. As Ashwini Kumar Lal writes of the first forms of life,

  Many of them are evolutionary relics called “archaea”, believed to be among the first homesteaders on the Earth 3.8 billion years ago. They are presumably
  the first version of life on our planet when its atmosphere was devoid of oxygen, and comprised largely of ammonia, methane, water vapour and carbon dioxide. They are microorganisms similar to bacteria in size and simplicity of structure, but continue as an ancient group intermediate between bacteria and eukaryotes. Heat – loving microbes, or “thermophiles”, are among the best studied of the extremophiles that can reproduce or grow readily in temperatures exceeding 45º C, and some of them, referred to as “hyperthermophiles”, are capable of thriving even thrive in temperatures as high as 110º C – more than boiling water temperature.

While we do not know (and may never know) the truth of this hypothesis, it is certainly plausible, given the locations where some extremophiles have been found.

References:

1: Microbial Life in Extremely Hot Environments

2: http://en.academic.ru/dic.nsf/enwiki/18641 (link no longer works, for some reason)

3: Origin of Life

Note: While I list several Wikipedia articles throughout the answer, I did not use them for the information in this answer. I think they're a good starting point to lead you to other sources, though.


Is there anyway from which we can measure the viscosity of honey using a refractometer?

Theoretically, if refractive index and viscosity are both simply functions of moisture content, you should be able to use one to approximate the other using an empirical standard curve. However, based on this paper, it looks like the relationship between moisture content and viscosity at 25C can vary quite a bit between different types of honey, expecially down below ~18% moisture. So I'd be pretty hesitant to rely on refractive index for acurate viscosity measurements unless you first rigerously validate your methodolgy against empirical viscosity measurements.


What is causing my problem with very low yields when isolating a 42kb yeast plasmid?

A dependable protocol for yeast DNA extraction I used to use was broadly similar to the protocols you cite but included an ethanol precipitation before and after the P:C extractions. The only expensive material was time. The general outline was:

Alkaline lysis
Ethanol precipitation
RNase A treatment of resuspended DNA for 15 minutes
Phenol:chloroform extraction (x2)
Ethanol precipitation

You probably know that the ethanol precipitation lore is that the yield is better the longer and colder you do your ethanol precipitations. I only ever did reverse transcriptase reactions a few times, but the template DNA I prepared spent the night in ethanol at -80C to maximize yield. Another place to double-check is that your yeast cultures are sufficiently dense before starting.


Is some of the energy of food lost during digestion?

Typically, catabolic reactions such as the hydrolysis of food stuffs into their monomers is an exothermic process. This includes conversion of proteins into amino aids, starchs into monosaccharides and fats into fatty acids plus glycerol. As an example, hydrolysis of a peptide bond linking the amino acids in a protein liberates 8-16 kJ/mol of energy.
https://en.wikipedia.org/wiki/Peptide_bond

So, that means a certain amount of the energy in food is liberated in the gut. But this is very minimal compared to the amount yet to be liberated, and harvested, as the many other bonds in the monomers are further broken down during cellular respiration.

A bit of research from a few different sites suggests the gut temperature is not meaningfully higher that the core body temperature measured in, say, the anus or vagina. https://en.wikipedia.org/wiki/Human_body_temperature  Any heat liberated from digestion in the gut must be slow enough to be absorbed into the bulk of the body without accumulating in the gut.


As can be inferred from the Shanks et al. paper linked in the question: In molecular biology, "suicide plasmid" is a term that refers to a plasmid which is replication incompetent.*

Plasmids normally bear a sequence called "origin of replication" Ori which marks the plasmid for replication by the host cell. Plasmids that lack this Ori will not be replicated during cell division, and will become diluted away and/or degraded after a few generations. Hence the name: The plasmid will "commit suicide" by promptly becoming eliminated from the population of DNA molecules inside each cell.

Note that because not all Oris are universal, the same exact plasmid may be a normal vector in one species (eg. E. coli) and a suicide vector in another species (eg. P. aeruginosa) - which is logical: If a vector can't replicate in any species at all, how do you produce this vector in the first place? (there are ways, but they are laborious)

*: I am unable to find an authoritative source for this definition. The other two paragraphs are common knowledge.


What is the name of the species of this butterfly?

I'm not an expert, but it looks like a male "common mormon" or Papilio polytes romulus

https://species.wikimedia.org/wiki/Papilio_polytes_romulus


Get protein annotation from Uniprot out of protein mappings

This problem is discussed here. Apparently STRING IDs are in KEGG format but these can be mapped on to Uniprot IDs using information downloadable from here. I guess that it is either the protein.aliases data or the mapping_files data that you would need. The first link provides a Python script to extract useful info from the downloaded data. These are big downloads so I haven't actually tried this out myself.

Presumably once you have the STRING→Uniprot conversion done you can query Uniprot with the output as a batch request.

Good luck!


"Alternative sensation" is not specific terminology in neuroscience - it is just the noun "sensation" with a descriptive adjective "alternative." It just means that it is referring to a different sensation than whatever the "primary" one is.

Knowing what this term means in a given context depends entirely on that context, and may not have any relationship to other contexts.

Time-frequency refers to how something varies in time and frequency. In the context of stimuli, for example, an auditory stimulus can have different "tones" or "notes": those are different sound frequencies, and those frequencies can happen in sequence. To describe a sound visually, one will often present a 'heat map' showing when (time) and at what frequency that sound has energy. Touch stimuli can also have a time-frequency representation, where the frequency indicates the vibration speed of the touch.


Why do pigeons kill their chicks when touched by a human?

This is a story I have been told as well when I was a kid. Usually this is related to the foreign smell that the humans leave on the chick. However, this seems to be an urban legend, as birds have not a great sense of smell.

Snopes says about this:

  However, Mother birds will not reject their babies because they smell
  human scent on them, nor will they refuse to set on eggs that have
  been handled by a person. Many birds have a limited sense of smell and
  cannot detect human scent, or if they can detect it, do not react to
  it.

What can happen is that the birds returning to their nest which find the nest disturbed compared to the situation when they left might cause them to temporarily or permanently abondon their nest.

You can find this and more urban legends about birds here and here.


Dendrodendritic synapse through axodendritic synapse at same dendrite?

I'm not sure if you are asking if an axon that sends a signal to a dendrite would then be released from that dendrite to another dendrite?

I don't see how this is possible seeing as the dendrite is already paired with the axon and downstream of said dendrite there would be a neuron.

A dendrodenritic synapse is two dendrites of two different neurons in contact with each other. For there to be a signal an action potential must have been reached.

Synapse is a junction between two neurons where chemical signaling occurs, but it is not the definition of a signal occurring. If that makes sense.

It seems like you are confused on the location and anatomy of a synapse.

There wouldn't be an axodendritic synapse followed by a dendrodendritic synapse then the neuron. It would either be axodendritic or dendrodendritic. Now there can be multitudes of connections between neurons but I don't think that is what you were asking.

Edit: Seeing your edit makes your question much clearer.

If the signal from the axodendritic synapse excites the neuron enough to reach action potential then that signal would be sent out through its synapses, including the dendrodendritic ones. So I guess in this way it was a "consequence" of the axodendritic synapse.

Though I would rather you think about it in that the action potential of one neuron sent a signal through it's connections to the neighborhing neuron, thus causing that neuron to reach action potential and further send out the signal. It's not really a "consequence" of the synapse, the synapse is more a pathway for the signal to travel.

The stimulus for the action potential is what causes a signal to fire and travel through a synapse.

Hopefully that answers your question.


Short Answer: Probably, at least a little, much research still needs to be done.  For a great paper on this see here.

Your question can be answered in two parts:

Can Epigenetics be inherited - The answer to the simple question in your title, do chromosomes change with time, is yes.  There are copying errors, and carcinogenic mutations that can permanently change cells' genomes.  Less permanent is epigenetics, which are temporary chemical modifications to the DNA which changes how it is expressed. The epigenetics of the cell may change for various reasons from the cell undergoing mitosis to a wildly changing diet.  However, when sperm and egg cells are formed these epigentic modifications are typically wiped from the genome in order to remove any possible damaging marks.  However, there is a growing body of literature which states that some marks escape the purge and change the characteristics of the progeny.  Studies include scare-treating mice, 1836 famine, fatty rats, human psychological changes.  While the exact genes causing the change is unknown, there is clearly a strong correlation
Can Music Skill be Captured in Epigenetics - Music skill is to difficult to measure biologically, but likely has some links in speech skills, which would be captured in the brain, and muscle skills.  While there is some evidence for there being an muscle epi-memory, brain epigenetic inheritance is more tenuous (although see this exciting paper on RNA causing memory changes through epigenetics).  I would say the general scientific consensus is that there is some relation between epigentics, and memory, and music skill - there is a great deal of work still to be done.


Spiders are naturally attracted to areas where preys are abundant, insects are primary source of spider prey. So you must create proper environment for insects in your home,  lights to attract nocturnal insects, flowers to attract butterflies and moths are attracted towards decaying vegetation(It may make your place smelly). Once insects are abundant then spiders are attracted towards these areas. Some parasitic wasps are predator to spiders like those belonging to Ichneumonidae, try to avoid these species. Also you can collect spider eggs and place it inside your home, so they will hatch out in your place.Some times you can see web full of spider nymphs, take it out and place it in your home.
Attracting spider to home can be achieved through buying some spider traps like poison free spider glue, which contains pheromones. Spiders are attracted to it and they will stick on them and eventually die, so you need to be careful and use the phenomenal effect of the spider trap to attract spiders or it will be dead and become useless.
The analysis revealed that the wasp spider pheromone is methylcitric acid trimethyl ester, a derivative of citric acid.
Some other techniques to attract spiders

An unspecified Cheiracanthium species is attracted to the smell of petroleum and has caused problems by weaving webs inside the canister vent of particular models of Mazda vehicles, resulting in blockages and build-up of pressure that could potentially cause fuel leakage from the fuel tank and an increased risk of fire. Mazda issued a voluntary recall of Mazda 6 models built between 2010-2012, to fit them with software which would alert drivers if problems were developing.
Reference

A spider that preys on the malaria-carrying mosquito is attracted to the odour of people's smelly socks, say scientists.
Reference

Eugenol baited traps we found seven individuals of two species of Thomisidae. In contrast, with the control traps, no Thomisidae were caught . Since Thomisidae were caught only in traps baitedwith eugenol, whereas no crab spiders were attracted to control traps, we postulate that eugenol served as an attractant for these spiders.
Reference


How do biologists estimate that there is 8% of protein coding genes in human genome?

S/he's off by about 6 - 7%.

As per the national human genome research institute approximately 1% of the human genome encodes proteins. We can tell this by looking at the sequence (which we're now able to do quite quickly) and identifying those portions of the sequence can be translated to protein using the genetic code.

  Scientists have been able to identify approximately 21,000 protein-coding genes, in large part by using the long-ago established genetic code. But these protein-coding regions make up only approximately 1 percent of the human genome...


What is the name of the plant with the down-falling light purple leaves?

It is a Digitalis purpurea

From the wikipedia page:


Papain is a cysteine protease, for which Wikipedia should be sufficient:

  Cysteine proteases play multi-faceted roles, virtually in every aspect of physiology and development in plants such as in growth and development, in senescence and apoptosis (programmed cell death), in accumulation and mobilization of storage proteins such as in seeds. In addition, they are involved in signalling pathways and in the response to biotic and abiotic stresses. In humans they are responsible for apoptosis, MHC class II immune responses, prohormone processing, and extracellular matrix remodeling important to bone development.


No, they can not do this. We don't have the enzymes to metabolize H2S, besides that, it is highly toxic. H2S can be used by some bacteria and archea (so called lithotrophic bacteria), but they are relatively rare.

Sulfur is reduced by plants, which take it up in the form of sulfates and subsequently reduce it to form different sulphur compounds. Animals are dependent on the uptake of sulphur from plant sources, as the sulphur containing amino acids are essential (meaning the cannot be synthesized by themself). The pathway is relatively complex. The image below is from the Wikipedia article on Sulphur assimilation, which I can also recommend, if you want to know all the details.


This is a Buprestid beetle, and I think the species is Chalcophora mariana. It doesn't look all that coppery in your photos, but the large size and shape is perfect. Their larvae live mostly on pines, so perhaps there were pines close to your meadow?  (Image from Wikipedia)


Why don't chromosomes double in S-phase?

First, chromosomes are composed of an original and a replicated chromatid, called sister chromatids. Chromatids are composed of tightly packed DNA.

DNA is replicated after the end of the S-phase, or in other words, the material composing the two sister chromatids is there. The catch is that chromosomes and chromatids aren't actually condensed yet, the DNA is still completely unpacked at this stage. So in fact, while you do not see actual chromosomes, the material composing them has been duplicated during the S-phase.

DNA condensation occurs two steps later during the prophase, where distinct sister chromatids/chromosomes are then formed from the packing of DNA that was duplicated during the S-phase.


Is galvinoxyl antioxidant assay possible using NMR spectroscopy?

Galvinoxyl is a free radical, which means it has an unpaired electron that can be detected with EPR. Antioxidants reduce the radical, which is then not detectable in the EPR anymore as it doesn't have an unpaired electron. What you need the EPR for in the assay is to determine how much of the galvinoxyl is still a radical.

Paramagnetic molecules like galvinoxyl are problematic for NMR, they bleach signals in close proximity to the radical and cause line-broadening. You still might be able to quantify the amount of oxidized and reduced galvinoxyl, but I'm not sure how reliable this would be. The oxidized galvinoxyl would probably be not visible in the NMR, while the reduced version would give a signal. You'd have to measure a few spectra to see if you can determine the percentage of reduced galvinoxyl from the NMR spectra.

EPR is the far easier method here, while I don't think doing this with NMR is impossible, there are quite a few ways it could be inaccurate. I'd strongly recommend to either use an EPR machine somewhere else, or use an entirely different assay that doesn't require such specialized equipment. I have no experience with antioxidation assays, but I'd guess that some exist that don't require EPR.


Strand representation in the DNA version of the Genetic Code

The sense strand has the same sequence as the transcribed RNA. The antisense strand is read in the other direction. For a particular gene, the sense strand is the genetic code, the other strand is the complementary template used to transcribe the RNA from it. The resultant pre-mRNA molecule (before introns are spliced our) will be single-stranded in the 5’ to 3’ direction with exactly the same sequence as the coding sequence (except for U instead of T). As such, the sense strand is the coding sequence of a gene (as it corresponds directly to the transcribed RNA sequence).

It is important to distinguish the direction of a DNA sequence. Genes can overlap in opposite directions. DNA and RNA molecules can only be synthesised by enzymes in one direction. This is important for DNA synthesis in vivo  (e.g., Okazaki fragments) and molecular biology experiments in vitro (e.g., PCR and NGS). Antisense RNAs are also expressed and are important in regulating cellular functions: this includes enhancers which sometimes express bi-directional RNA and short RNAs involved in RNA interference, microRNA, and CRISPR-Cas).

In molecular, cellular, and computational biology, the sense strand encodes the coding sequence (gene or other transcript). This is the sequence of any resulting RNA. Hence we define a codon as the nucleotide triplet that corresponds to a resulting amino acid. The antisense DNA strand and the tRNAs are complementary to this. Therefore there is an agreed upon convention to determine which strand is “coding” and it is straightforward to derive the resulting amino acid sequence of the encoded peptide given a coding sequence and a start codon (AUG). The antisense strand is the reverse compliment sequence which can also be computed. It is not necessary to store the sequence of both strands of a gene since the coding sequence can be used to infer the sequence of both strands.

See Figure 6-7. Molecular Biology of the Cell. 4th edition. Alberts B, Johnson A, Lewis J, et al. New York: Garland Science; 2002. excerpt online


1) This is a bit simplified; in reality, flashes of light or dark that cover the whole receptive field do influence the firing rate somewhat, just not nearly as much as an on-center stimulus for an on-center RGC. Your textbook is using a bit of an idealized interpretation to convey the concept of center-surround organization. I'm not sure what your confusion related to the horizontal cells is, however.

2) This is usually called "adaptation" and is a general principle in nervous systems (particularly on the sensory side). Multiple systems influence adaptation, including depletion of neurotransmitter-containing vesicles, metabotropic receptors activated by high concentrations of neurotransmitter that have opposite-sign effects to ligand-gated receptors, feedback systems that suppress the potency of second-messenger systems, accumulation of extracellular inhibitory neurotransmitters, etc. For the eye, there are additional sources of adaptation that come into play, depending on the experimental paradigm.

Without knowing the exact paradigm your textbook is meaning to indicate, it's probably more important at this point to just recognize adaptation as a normal aspect of sensory processing. The specific mechanisms can be understood later.

3) Yes - but you don't need to go to anything as complex as an artificial neural network. Basic image filters like the Laplacian of Gaussian (LOG) filter are basic approximations of center-surround organization in the retina.


Why do floaters in the human eye appear to have a squiggly-line, tubular shape?

Eye floaters are usually small flecks of collagen floating inside of your eye (the same substance that is present in the extra-cellular matrix) and as you age they can clump together and cast shadows on your retina.
They may look like microbes to you because the clumping gives the appearance of a thread-like or rod shape, commonly associated with microbes. The light falling on the eye will enhance this by making them look transparent and somewhat like microbes. But rest assured they aren't, because if they are, then you certainly have superhuman eyes!


If human proteins are synthesized from only 20 different amino acids, then how can there be such variety of proteins in human cells?

There are only 26 letters in the English language, and more than 80% of words are under 10 letters. Yet there are over a million English words. Nonsense words don't count.

Now imagine the possibilities of a 20 letter alphabet, where the average "word" length is about 375 letters, and where words of up to 800 letters are possible. And that also does not include "nonsense words".

That should give you an idea of the possibilities, and why "thousands of different proteins in human cells" can exist.

How big is the “average” protein?


There are physical limits to the existance of life forms, wether temperature, pressure, osmolarity, etc. But these are usually physicochemical fields acting over a wide spatial structure. In the case of drugs, they are physically localized molecular entities. They are usually very tiny, even compared to the smallest microbes. Even though the genome of any microbe is finite and they could not, in theory, recognize the infinitely many drugs we can synthesize (assuming the simple case they need one gene per drug resisted), they can just evolve very generic mechanisms like preventing these molecules to get into the microbe, pumping them out of the cell, or other generic mechanism; with the same overall effect: preventing the drug from acting in the desired way.

The question you ask is very interesting, and it is the focus of some recent efforts and discussions among academics. Here you can find a recent article discussing the possibility of "evolution-proof" drugs. As you can see, the subject is not trivial.

Cheers,

Pedro


Check the "dark background" checkbox that is unchecked if the background is dark and you want to select the bright cells. Right now it is assuming the background is bright.


How can ionized amino acid form be important for the catalytic activity?

Enzymatic reactions are chemical reactions. Chemical reactions involve charge ("electron") transfer. Charge transfer occurs more readily if there is a large gradient in charge density between the attacking active site group and the attacked atom of the substrate. Many enzymes (yes, it is really quite common) use ionic forms of aspartate or glutamate as a catalytic amino acid residue.

For example, some enzymes belonging to the alpha/beta-hydrolase fold family (e.g., haloalkane dehalogenases, epoxide hydrolases) use a deprotonated aspartate as the nucleophile (which attacks an electrophilic atom of the substrate); the specific position of the nucleophile within the enzyme and its interaction with other groups in the enzyme enhance the nucleophilic nature of the aspartate, a phenomenon called "oxyanion hole."

Ollis et al. (1992) Protein Eng 5: 197-211.
https://www.ncbi.nlm.nih.gov/pubmed/1409539


Implanted neural recording system vs Electroencephalography

EEG records a rough average of activity from a large area of the brain, because it is located far away from the actual neurons. There is no way to separate out the activity of individual or even small groups of cells; instead, you record lower frequency synchronous activity among whole populations.

Implanted systems can record from small groups or sometimes even single neurons, which greatly increases the amount of information available.

Depending on the purposes of the recording or research, EEG might be sufficient; in other cases, implantable electrodes are required. EEG is sufficient to monitor sleep/wake cycles, for example; there is no need to record intracranially to monitor sleep (unless perhaps you are studying mechanisms of sleep itself). Implanted electrodes are often used before surgery to remove parts of the brain that are causing seizures. Using ECoG (basically an "EEG on the dura" rather than on the skull) or depth electrodes allows the surgeon to know more precisely which area is causing seizures, hopefully leading to a more successful surgery and needing to resect less tissue.

Implanted electrodes are also commonly used in animal experiments to learn about how single neurons and small populations encode or process information.


What is meant by increase in information embodied in the system?

Table 1 on the next page (p. 36) lists a number of properties for each of the three "growth forms".

For information, properties include:

Life history types
Diversity (taxonomic & ecological)
Body size
Stability

I have to admit that some of these properties doesn't really make sense to me under these headings (at least from the common use of these terms). However, I suspect that they are used in a very specific sense that might make sense if you read the entire book. And systems ecology isn't really my thing.

Note also that exergy (which is used in relation to these three growth forms in the book) is a term borrowed from thermodynamics (ie physics), and it describes potential/available work. Exergy is also negatively related to entropy, so when exergy decreases, entropy increases. Since higher entropy is related to disorder, the opposite goes for exergy, so high exergy means a higher amount of order (within the system), which can be translated into "structural information". I suspect that this is the form of information that the book is referring to, as one of the "growth forms".


Can the human body create glucose out of fat?

Only about 5–6% of triglyceride (fat) can be converted to glucose in humans.

This is because triglyceride is made up of one 3-carbon glycerol molecule and three 16- or 18-carbon fatty acids. The glycerol (3/51-to-57 = 5.2–5.9%) can be converted to glucose in the liver by gluconeogenesis (after conversion to dihydroxyacetone phosphate).

The fatty acid chains, however, are oxidized to acetyl-CoA, which cannot be converted to glucose in humans. Acetyl-CoA is a source of ATP when oxidized in the tricarboxylic acid cycle, but the carbon goes to carbon dioxide. (The molecule of oxaloacetate produced in the cycle only balances the one acetyl-CoA condenses with to enter the cycle, and so cannot be tapped off to gluconeogenesis.)

So triglyceride is a poor source of glucose in starvation, and that is not its primary function. Some Acetyl-CoA is converted to ketone bodies (acetoacetate and β-hydroxybutyrate) in starvation, which can replace part — but not all — of the brain’s requirement for glucose.

Plants and some bacteria can convert fatty acids to glucose because they possess the glyoxylate shunt enzymes that allow two molecules of Acetyl-CoA to be converted into malate and then oxaloacetate. This is generally lacking in mammals, although it has been reported in hibernating animals (thanks to @Roland for the last piece of info).


What is the Giemsa staining of chromosomes?

Giemsa is not a particular methid to stain malaria or any other parasite. It stains DNA. As such, it can be used to stain any DNA-containing organism, or, in other words, any known cell.
Regarding its particular use in chromosomal banding, you can refer to many online resources, such as this one of the University of Washington:

Chromosomes in metaphase can be identified using certain staining techniques, so called banding
(...)
G-bands are most commonly used. They take their name from the Giemsa dye, but can be produced with other dyes. In G-bands, the dark regions tend to be heterochromatic, late-replicating and AT rich. The bright regions tend to be euchromatic, early-replicating and GC rich.


How specimens are organized in a large biological specimens archive

Biological specimens are ordered in museums phylogenetically. So all the birds are in one place, and the insects in another. Fossils are generally kept in their own place. Different museums may have their own standards, but most sort specimens phylogenetically as well. But alphabetical sorting also happens. So that all the members of a family are in one place, and then the genera within the family are organized alphabetically. So all the Trichoptera (Insecta), for example, at the Smithsonian are together on one of the floors with other insects, curated by a Trichoptera specialist. Within Trichoptera, the first drawers are Apatanaeidae, and the last are Xiphocentronidae. Individual specimens are often given a unique number, usually sequential, with the time of accession into the museum.


Why does shaving dehydrate the skin? Is there an hormonal effect involved?

First of all 'Testosterone' hormone controls the growth of hair on our body and also oil secretion. Depending up on the nature of a person's body, this hormone controls the growth of the hair.

Why shaving facial hair leaves the skin dry ?

First let me explain the reason behind the oiliness of the skin. Sebum is produced by the sebaceous glands and is a complex made up of cholesterol, free fatty acids, glycerides, squalene, and wax esters. Sebum and sweat, along with the epidermal lipids discussed earlier, make up the oil on the surface of the skin. Some people will have more oily skin and some have less which depends on the nature of body.

While shaving the sharp razor cuts the hair and also damages the skin and hair follicles. The level of damage to skin also depends whether you are shaving downwards or upwards. Because upward shaving usually causes more damage to skin and hair follicle. Complete detail of damage to hair follicle can be found in this article: Science of shaving.

Shaving also removes skin lipids and water content creates pores which exposes the skin. If the surrounding atmosphere is dry then skin loses water. Or if the surrounding is moist or humid then water content will be balanced. That is the reason why we use artificial face moisturizer for immediate remedy to avoid infection and balance the wetness of face. So it takes a while for the skin to get back to normal state if nothing is done after shaving which sometime leads to acne or rashes due to infection.

Another reason for dry face is use of hot water which removes skin oil instantaneously. So lukewarm water or cold water will further reduce the dryness of the skin. (Use of shaving cream with high alkaline content will obviously result in dry skin. This holds for soaps also.)

Complete details can be found in the first link provided and Drying skin after shave.


What is the difference between fixation and loss of alleles in a population?

Yes, 'lost' seems to be referring to fixation of the a allele in this program, where the statements 'fixed' and 'lost' are specifically referring to the A allele. Conceptually, 'fixed' and 'lost' are describing the same thing in this particular case ( since you only have two alleles in the population) - the loss of one allele in a population.

  Note that once the plot of the gene frequency curves reaches the right-hand side of the graph, the program prints there the number of populations that fixed for the A allele (ended up with a frequency of 1.0) and the number that lost this allele.

(my emphasis, from http://evolution.gs.washington.edu/popgen/popg.html)


Sure, I can identify this for you!

That is an Argiope Aurantia, most commonly known as a "Yellow Garden Spider". They're quite well known for the design of the webs they spin, and because of this, they also go by "Sewing Spider" and "Writing Spider". They may try to bite if startled (which can be easy to do), but their venom is harmless to humans, so no worries.


What are ways to compare the "costs" and "gains" of food production systems?

Calories and dollars are the most obvious and straightforward, but including additional variables complicates the accounting. . A great paper that used energy has been updated in a more recent publication. Emergy is an interesting alternative.

Current work includes the Natural Captial project that "aims to integrate the values of nature into all major decisions affecting the environment and human well-being". Of course, this approach exchanges a simple currency for a more comprehensive one.

Climate regulating value is also a relatively straightforward and relevant currency that can be used to compare the value of food production systems.


What are these near microscopic white bugs from my comb?

Those look like they could be dust mites and are certainly some sort of mite. Dust mites are found everywhere in homes and are around 0.2 mm in length.

Dust mites image by Gilles San Martin:

Dermatophagoide pteronyssinus (European house dust mite):

Dermatophagoides farinae (American house dust mite):

You can learn more about dust mites from the BBC and the US NIH.


Book recommendation on mammal (or just primate) behaviour, especially in relation to child-rearing

Suggested Reads:

Evolutionary Psychology

By Lance Workman, Will Reader

Evolution of Human Behavior: Primate Models

edited by Warren G. Kinzey

Social Behaviour of Children: A Cross Cultural Assessment

By Ralph E. S. Tanner


Is there a good field methods book that covers terrestrial ecology?

Take a look at Field and Laboratory Methods for General Ecology by James E. Brower, Jerrold H. Zar, and Carl N. von Ende.

If you are only interested in plant sampling techniques, an great resource published by U.S. Bureau of Land Management is Measuring & Monitoring Plant Populations by Caryl L. Elzinga, Daniel W. Salzer, and John W. Willoughby.

Another great resource that covers wildlife research and management techniques (2 volume set) is The Wildlife Techniques Manual published by The Wildlife Society and edited by Nova J. Silvy.


What is the name of this plant, from Bangladesh?

This plant belong to Malvaceae, and the yellow flowers open towards morning to mid-day.
This plant is most-likely Sida rhombifolia or may be Malvastrum tricuspidatum .
From broad leaves it seems not Sida acuta
Check epicalyx ( made up of bracteoles)... is there is no epicalyx then Sida rhombifolia.
If epicalyx is 3, it is Malvastrum tricuspidatum
look also https://en.wikipedia.org/wiki/Sida_rhombifolia,
https://books.google.co.in/books?id=Roi0lwSXFnUC&lpg=PA258&ots=N7DNvrN4UL&dq=malvastrum%20tricuspidatum%203%20epicalyx&pg=PA258#v=onepage&q=malvastrum%20tricuspidatum%203%20epicalyx&f=false
Epicalyx of Malvastrum tricuspidatum :

C= Corolla (all petals), K= Calyx (all sepals), E= Epicalyx the bracteole

3 bracteoles


How do some plants grow in salt water, while others die?

A few things you have to realize when you ask 'why hasn't species x evolved trait y':

What is the cost of evolving this trait? If you gain one trait, you lose another (or others). Everything in evolution is a tradeoff: that's why you're not nine feet tall, you'd be able to beat up all your enemies great, but it would take so much food to sustain you, it wouldn't be worth it.
Not every trait can be easily evolved. When you're starting as a freshwater plant, there are many, many, many, many mutations that have to occur for you to become salt-tolerant. Every one of those mutations would have to give a fitness advantage to be positively selected. The chances of this happening are low, which means if it happens at all, it would take a long time.
Who knows, perhaps these plants are, slowly, becoming more and more salt-tolerant and you're seeing them at an intermediate point in their evolution. Everything is evolving all the time, if these plants were not in a salty environment until recently, mutation and selection haven't had time to work their magic.

Update from comment:

  Can you flesh out a little on "How can the plants keep from intaking salt, while absorbing other soluble nutrients through the roots?"

Sure! I'll give you the simple answer first: there are different mechanisms for absorbing salt and for absorbing nutrients, so they can function largely independently.

Now the longer explanation: Salt and nutrients don't just diffuse (much) through cell walls, they have to be transported across by what are called transmembrane proteins. Think of the cell membrane (a layer inside the cell wall) as basically something like a layer of oil (it's called a lipid bilayer) -- you know oil and water don't mut, and for the different ions in salt (sodium ion and chloride), neither do oil and salt or oil and many nutrients so they get sort of escorted across that barrier by big proteins that form sort of a tunnel through it.

There's a different transport protein for different substances; the salt ones will only let salt through, and in fact there are different ones for letting salts in and letting salts out, and for the different ions (sodium and chloride) in salt.

Update from comment:

  This makes me wonder how salt harms most plants, if it can't get in except by 'invitation'

Quite a bit of salt can diffuse in, the molecules are small enough (unlike most nutrients) to pass through the membrane via the channels that let water in. Every living creature has a quite sophisticated setup of "ion channels" to pump salt out. If suddenly its cells are in a very salty environment, these pumps can't keep up.

Update from comment:

  So if salt can diffuse in, what do salt-tolerant plants have that other plants don't?

Mostly, if I recall correctly, three things: They will have enzymes that have evolved to work in higher salt concentrations, they will have cellular functions to "sequestrate" salt, i.e. store it in organelles called vacuoles instead of leaving it where it can harm other organelles, and of course they will expend more resources on ion pumps to get the salt concentration in the cell to an acceptable level.


How do alcohols and aldehydes destroy the plasma membranes of bacteria?

Alcohols are dehydrating - they remove water from the cell. And since cells need water to survive, this is lethal to bacteria. However, in order to work effectively, an alcohol needs the proper amount of time to penetrate the cell membrane of the bacterium. If the percentage of alcohol is too high, it will evaporate before entering the cell. Too low, and it will enter the cell but not be lethal. 70% alcohol turns out to be the most effective concentration for use as a surface disinfectant with many different types bacteria.


Why aren't the twin organs like both the eyes, ears, hands and legs lying both sides of a human body identical?

The topic you're looking into is fluctuating asymmetry, a broad field of study.  Among the free reviews this one is a bit old but well on topic.  The general idea is that there is "developmental noise", which is opposed by mechanisms for developmental stability.  The review covers a variety of conclusions people try to read in to these studies, often about the stresses on the organism or the mechanisms by which development is "canalized" to reach a specific goal.
The nature of the noise is usually presumed rather than proven, since many different factors are presumably adding up to make small differences.  We may assume (though I'm not always sure it is true) that mRNA, protein, and signalling molecules diffuse to reach their targets, which is to say they are subject to Brownian motion with random variations in timing.  The need for multiple factors to get together for a complex process like transcription or translation means that the number of copies of a protein produced under a given circumstance will vary.  An example of this in hypertrophic cardiomyopathy has been proposed to contribute to disease progression, due to random bursts of transcription in individual heart cells affected by the disease.


When a thought 'crosses your mind', does it literally cross between left and right cerebral hemispheres?

Neuroscience doesn't really have a clear model for what a "thought" consists of exactly. Certain processes that are involved in thought have begun to be mapped--for example, this recent paper talks about a model for how the brain associates location in space with it's own mental map (http://www.ncbi.nlm.nih.gov/pubmed/24462102, I'll try to find something related that's not behind a paywall...). This one doesn't address your particular problem though, they only measured activity on one side of the brain. So basically, it might be possible to partially answer your question for more specific brain processes, but different kinds of "thoughts" are processed in different ways.

And of course I am also conflating impulses crossing the corpus callosum with the thoughts themselves, but I don't think this is really accurate. The most popular models in the labs I'm familiar with suggest that a "thought" is composed of a bunch of neural activity taken together rather than the activities of a few neurons on their own. But that might ultimately just be arguing semantics.


Why is the Pentose Phosphate Pathway so active in erythrocytes?

No. Your supposition is incorrect — the phosphate in glyceraldehyde 3-phosphate has to come from somewhere, and it comes from glucose 6-phosphate. The reason a second ATP is required before you get to the triose phosphate stage in glycolysis is that you are generating two molecules of triose phosphate. In the pentose phosphate pathway (energy-producing non-oxidative branch) you are not generating two molecules of triose-P from one hexose-P, you are generating two hexose-P and one trisose-P from three hexose-P, as shown in my Diagrams 2 and 3 below. (The other three carbon atoms are lost as CO2.)

A good way of approaching this question is to ask “What can be produced by the pentose phosphate pathway that cannot be produced by glycolysis?”.

Glycolysis may be summarized in this context as:

  Glucose + NAD+ ➝ Pyruvate + NADH + 2ATP

But to allow glycolysis to continue the NADH is reoxidized to NAD+:

  Pyruvate + NADH ➝ Lactate + NAD+

So the sole product of glycolysis for the erythrocyte is ATP (primarily for active cation transport to maintain cell shape) lactate passes into the blood for recycling.

The Pentose Phosphate Pathway (the oxidative stage) is shown in Diagram 1, above, and may be summarized in the way done for glycolysis as:

  Glucose + ATP + 2NADP+ ➝ Ribulose 5-P + CO2 + 2NADPH

Ribulose 5-P has two possible fates, but only one differs from glycolysis, so the two distinguishing products of the pathway are ribose and NADPH.

Ribose is important for nucleic acid synthesis, particularly in dividing cells, explaining the increased activity of the pentose phosphate pathway in those cells. This cannot be the reason for the high activity of the pathway in erythrocytes as they have no nuclei and do not divide. In fact the ribulose 5-P is fed back into glycolysis for generation of ATP as shown in diagrams 2 and 3.

NADPH, then, is the answer in this case. It is the reducing agent used in the cytoplasm for synthetic processes (unlike NADH used particularly for ATP generation in the mitochondria), and so the pentose phosphate pathway is found in cells such as adipose, mammary gland and liver, that synthesize fatty acids, and cells that synthesize steroids. However that is not there is no fatty acid or steroid synthesis in the erythrocyte.

NADPH is important in erythrocytes as it is the specific source of reducing power required to keep the molecule glutathione in a reduced state. This has an important protective role in reducing cellular molecules that have become oxidized by molecular oxygen, a problem that is more acute in erythrocytes than in perhaps any other cells as they are the carriers of molecular oxygen. The cell membrane is particularly prone to oxidative damage. You can read about this online in this chapter in Berg et al.


Is this a termite wing or flying ant wing

This appears to be the wing of a crane fly (Tipulidae).  Using this figure you can begin narrowing down the possibilities for wing venation. Searching diptera wing venation, I think, brings up this excellent diagram (see bottom left for Tipulidae) which quite closely matches your photo if rotated in a graphics program (GIMP):

 Wing photo from OP paired with wing outline image copied and rotated from Batsdiet.com
You could likely drill this down further by searching Tipulidae venation or the like on Google Scholar, which pulls up many papers with detailed information on various regions and taxa of crane flies.


Skin is composed of layers, the uppermost being the epidermis. Upper layers of the epidermis (dry, flat cells tightly packed together, and of varying thickness on different parts of the body) can be abraded off, leaving deeper layers of the epidermis (nearer to underlying blood vessels) exposed. Since peripheral nerve endings do exist in this area, the wound is painful. A wound that does not extend into the dermis does not bleed (for example, a second degree burn can lift the upper layers of the epidermis from the deeper layers; no blood will collect in the blister, but the wound is painful. Peel off the top of the blister, and you have an analogous situation.

Because the surface of the skin is no longer present, fluid (as with a blister, not containing red blood cells) leaks from the blood vessels. Initially a transudate, it can also be an exudate. And, no, it does not contain the cells needed to regenerate the upper layers of the skin. It contains many of the proteins found in serum and may contain white blood cells which help to fight off infection.

New cells are generated from the deeper cell layers (the basal cells) which are still intact. They grow from the bottom of the wound up, so to speak. The scab formed by the dried fluid keeps the layer under it moist, providing a good environment for cell growth.

Epidermis and Its Renewal by Stem Cells


Is diarrhoea advantageous to the microbe?

Vibrio cholera for example is actively causing diarrhoea, by stimulating the CFTR channel to excrete chlorine ions, which will attract water from the gut tissue.

The answer of the function seems obvious: to promote dispersal in the environment and as such infect/find new hosts.
See also: extended phenotype (Richard Dawkins): how genes in one organism (mostly a parasite) influence the behaviour of another organism (mostly the host of the parasite) to increase the (reproductive) success of the gene/parasite.
Also: numerous (some horrifying) examples in Parasite Rex (by Carl Zimmer)


What is solid-phase bridge amplification?

This stage is after the adsorption of the adapter-ligated fragments on the flow cells.
The fragments are isothermally amplified to generate clusters [1]. The exact nature of the enzyme mix that catalyses this step is not disclosed by Illumina. I assume it must be similar to Helicase mediated isothermal amplification, which uses helicase and single strand-binding proteins (SSB) to denature the template. The polymerization is catalysed by a mesophilic DNA-Pol such as Klenow (E.coli).


High salt environments are strongly hypertonic and disrupt the osmotic gradients of cells.  Excess salt gets forced in (disrupting function) and cell water gets drawn out.

In simpler terms, it dehydrates them.

This link has more info regarding what is required to live in high salt environments (and by corollary, why organisms without such features die):

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


How does DNA from sperm fuse with DNA in egg?

First, to clarify on the number issue and parental origin of the chromosomes. For the moment, disregard crossing over. Then, you would begin with an adult somatic cell in the growth phase, having 46 chromosomes, two of each kind, that is, 23 pairs (assuming sex chromosomes to be of the same kind, including the case in males). Then, in the S phase, each chromosome replicates, creating exactly similar sister chromatids, each of these sisters being similar to the single chromosome the cell had in growth phase. Each of these chromosomes with two chromatids, sends one to each daughter cell, making the daughter cell exactly like their parents. In meiosis, after this step, one of each kind of chromosome separates into a gamete, so that instead of 23 pairs, each gamete has only 23 chromosomes, one of each kind. On fusion of two gametes, you would have the original configuration again.

Crossing over, just means that when the two chromosomes of a particular kind separate during meiosis, they exchange corresponding material. If no crossing over happened, the gamete would either have one of the two same-kind chromosome, or the other. But due to crossing over, you create a different set of genes on these two chromosomes, different from the ones fond elsewhere in your body. So if say two chromosomes of the same kind have genes $ABC$ and $DEF$, if no crossing over happened, the gamete would have either $ABC$ or $DEF$. But crossing over makes possible combinations like $AEF$, or $DEC$ etc.


Why do I need a flu shot every year, while many other vaccinations last years or even a lifetime?

The flu virus changes rapidly so that the current vaccine doesn't work against the new strains.

The way vaccines work is that they teach our immune system what to look out for. The vaccine contains bits of the virus but in a form that can't cause a proper infection, the body learns what to look for and next time before the virus can really get going the immune system kills it off first.

In the case of flu, every year it looks different enough that the targeting mechanisms of our body don't recognise it. Flu being a RNA virus frequently mutates until it is slightly different. This is called antigenic drift, the changing of the antigens or the parts our body recognises.

On top of that there's lots and lots of types of the influenza virus, that can not only infect humans but others which affect other animals. Occasionally the virus might combine with a random other strain making it completely new: an animal flu and human flu hybrid. These are the epidemics of swine or avian flu etc. This recombination is called antigenic shift.

So each year scientists predict which viruses will affect us this coming year and grow them ready for vaccines. Of course there's some of the old virus floating around looking for someone to infect, but those infected can't be infected by it again if the immune system is working.


Did not understand a small excerpt from a research paper

The paper's description is poor, but they seem to be describing an encoding where each of 20 possible amino acids are associated with a position within a string of 20 bits, e.g. alanine with offset 0, cysteine with offset 1, etc.  With that representation, one amino acid residue within a window is encoded by a string of 20 bits, 19 of them being 0 and the other a 1; the single 1 bit occurring in the place corresponding to the residue.

This interpretation is supported by the paper's citation of  Qian N, Sejnowski TJ (1998) "Predicting the secondary structure of globular
proteins using neural network models." J Mol Biol 202: 865–884.  Qian's paper says:

  Each group has 21 units, each unit representing 1 of the amino acids (or spacer). For a local encoding of the input sequence, 1 and only 1 input unit in each group, corresponding to the appropriate amino acid at each position, is given a value 1, and the rest are set to 0.


What are the roles of guanidine-HCl and ethanol in binding of DNA to silica?

Guanidine HCL is a chaotropic salt.  Chaotropic salts are critical for cell lysis and binding to the silica resin. Specifically, Chaotropes have two important roles in nucleic acid extraction

Destabilize hydrogen bonds, van der Waals forces and hydrophobic interactions.

Leading to destabilization of proteins (including nucleases).

  Macromolecular structure and function is dependent on the net effect of these forces (see protein folding), therefore it follows that an increase in chaotropic solutes in a biological system will denature macromolecules, reduce enzymatic activity and induce stress on a cell (i.e., a cell will have to synthesize stress protectants). Tertiary protein folding is dependent on hydrophobic forces from amino acids throughout the sequence of the protein. Chaotropic solutes decrease the net hydrophobic effect of hydrophobic regions because of a disordering of water molecules adjacent to the protein. This solubilises the hydrophobic region in the solution, thereby denaturing the protein. This is also directly applicable to the hydrophobic region in lipid bilayers; if a critical concentration of a chaotropic solute is reached (in the hydrophobic region of the bilayer) then membrane integrity will be compromised, and the cell will lyse. [Source]

Disrupt the association of nucleic acids with water.

Thereby providing optimal conditions for their transfer to silica.

  Salts can have chaotropic properties by shielding charges and preventing the stabilization of salt bridges. Hydrogen bonding is stronger in non-polar media, so salts, which increase the chemical polarity of the solvent, can also destabilize hydrogen bonding. Mechanistically this is because there are insufficient water molecules to effectively solvate the ions. This can result in ion-dipole interactions between the salts and hydrogen bonding species which are more favorable than normal hydrogen bonds. [Source]

Ethanol, like Guanidine HCL, is a  chaotopic agent.  Ethanol is added for 2 reasons:

Enhance and influence the binding of nucleic acids to the silica.

Interfere with non-covalent intramolecular forces as outlined above.
Reduce association of nucleic acids with water. From Melzak et al. (1996):

  Decreaing the water activity in solution through addition of either a chaotropic salt or an alcohol changes the helical structureof B-DNA either continuously to C-DNA or through a sharp  cooperative transition to A-DNA (28). Either transition is  accompanied by a decrease in solvent-accessible surface  area.

The correct concentration allows for washing of the salts from the membrane. [Source].

Citations

Melzak et al. (1996) Driving forces for DNA adsorption to silica in perchlorate solutions. J. Colloid Interface Sci. 181: 635 - 644.


I'm answering this question (mostly) based on prior knowledge.

Inside the womb, the foetus relies on the mother for oxygen i.e. it receives oxygen from the mother's bloodstream via the umbilical cord.  A foetus doesn't use its lungs for breathing inside the womb. Ever.

Besides, lungs of a foetus are considered fully matured no earlier than the 36th week of pregnancy. (Though there are exceptions to this)

  During fetal life the baby's lungs are filled with fluid and they do not perform any respiratory functions. [1]

At birth, the baby is forced to breath on its own for the first time. Hence, the baby cries - or more precisely - gasps for air.
This 'cry' of the baby is actually a strong respiratory effort, thereby aiding the baby in its first breath. This is also why newborns don't produce tears on their first cry. Because it's not really a cry, it's a gasp for air.

Now the reason why such a considerable effort is required for the newborn to breathe is because:

A) Lungs are being used for the first time, and

B) The lungs of a foetus are filled with amniotic fluid when it's inside the womb. Effort is needed to push this fluid out from the lungs after birth.

I'm not aware if there's any genetics involved in this. I don't think there is.

Source: [1] http://www.thehindu.com/todays-paper/tp-features/tp-sci-tech-and-agri/babys-first-cry/article2267767.ece


Tumor ‘budding’ is loosely defined as the presence of individual cells and small clusters of tumor cells at the invasive front of carcinomas. A study of the measure of budding can give an insight into how fast the disease might propogate.

Reference


Why are "itch signals" transmitted so slowly from the skin to the human brain?

What causes the "itch" fibers to transmit signals to the brain so slowly? Is there thought to be some evolutionary benefit to such slow conduction, considering that the speed of most signals from skin to brain are transmitted so much faster?

The interview most likely refers to the findings of Schmelz et al., J. Neuroscience, 1997: Specific C-receptors for itch in human skin

In essence they found tested the sensitivity of unmyelinated nerve fibers (note: myelination also increases transmission speed) towards distinct stimuli. They found that some of those fibers would selectively respond to stimuli which would be perceived as itching (such as histamines). They find that:

  This slow conduction velocities attributable to small axon diameters ...

Note that since they don't need to, they also don't speculate on the physiological reason, why itching should be processed by slower fibers (and some potential explanations will be recognized quite well by readers of their article).

Please also note that the original claim, from 1997, however has been softened with the years, and there appears no strict separation been stimuli like "hot", and itching, in terms of distinct fibers and transmission speeds; e.g.: Davidson et Giesler, Trends in Neuroscience, 2011: The multiple pathways for itch and their interaction with pain


What would "N" and "V" stand for in DNA barcoding?

It is standard IUPAC nomenclature to write bases that are not uniquely defined.

For example, "N" means "any base", but "V" means "A, C or G, but not T".

See the full list here


You can put any media in a GasPak or other anaerobic system depending the type of anaerobic growth you are looking for. Sometimes blood is simply added to media to meet nutritional requirements of an organism. I use Columbia Blood agar often as a general purpose anaerobic medium. In a collection of 100+ obligate anaerobes I am working with, around half grow well on columbia agar with 5% sheeps blood, and many of those will not grow on Columbia without this blood amendment. As an added bonus, I can easily spot certain common contaminants growing on my plates by their hemolysis paterns.


Why is there no symmetry in pigmentation when comparing people north and south of the equator?

I rather would say that the lack of North/South Symmetry in pigmentation is that we forget how quickly human beings have spread. In prehistory, people have come to populate every continent over perhaps the last 60,000 years.

While in that time its clear that several mutations have popped up to influence skin color, they are pretty rare compared to the speed with which we migrated over the globe.  The dark color of our earliest ancestors has been lost and regained more than once, but not so often that the selection pressure of latitude have made indigenous in the tropics of south america or south east asia uniformly as dark as africans. Or for that matter have lightened the skin of pre-colonial South Africans.

One might guess that clothing and shelter have reduced the selection pressure on pigmentation further over the past few thousand years.

Individual cases should be studied - this is just a sketch - but the general thought here is that the pigmentation of human beings have more to do with where they have been and how quickly they have recently come from in their migrations.

Summarizing the comments below: There is a correlation between pigmentation and latitude.  The answer is really a combination of latitude, how long a people has been there, and the speed at which pigmentation mutants show up. It doesn't change so quickly that all people are equally dark at the same latitude or so slowly that you find completely pale people at the equator.