Is coral photosynthesis dependant on the wavelength or frequency of light?

Short answer: Coral doesn't need the light, it's the zooxanthellae that is symbiotic with some corals that relies on light to grow; it adapts to the frequency spectrum available at the depth the particular coral grows, full spectrum at shallow depths and at over ~30m the zooxanthellae relies on blue light because other frequencies are absorbed by water.
Some species of coral, such as Lophelia pertusa, grow in water so deep that there is too little light for them to rely on zooxanthellae, instead their polyps gather food directly with their tentacles, feeding heterotrophically.
There are even instances of coral feeding on jellyfish, see: "Opportunistic feeding by the fungiid coral Fungia scruposa on the moon jellyfish Aurelia aurita" (May 21 2009), by A. Alamaru, O. Bronstein, G. Dishon and Y. Loya
Longer answer:
The physics portion of your question is best answered on our Physics.SE site's question: "Why doesn't the frequency of light change during refraction?"
Light's wavelength and frequency are related to each other based on a mathematical formula, it's the intensity that is affected by passing through a medium; different materials will attenuate some frequencies more than others. Water doesn't transpose light's frequency or wavelength as much as it absorbs (filters) the frequencies of light affecting which color can penetrate deeper.

"What is a light wave?
Light is a disturbance of electric and magnetic fields that travels in the form of a wave. Imagine throwing a pebble into a still pond and watching the circular ripples moving outward. Like those ripples, each light wave has a series of high points known as crests, where the electric field is highest, and a series of low points known as troughs, where the electric field is lowest. The wavelength is the distance between two wave crests, which is the same as the distance between two troughs. The number of wave crests that pass through a given point in one second is called the frequency, measured in units of cycles per second called Hertz. The speed of the light wave equals the frequency times the wavelength.".

See this other Physics.SE question: "Does light color change when refracting?":

"The color will not change. What you're not taking into account is the speed of light in the medium. It's not the same $c$ en vacuo. The frequency stays the same. What changes is that speed of light in the refracting medium and as a result wavelength.".

Here is what sunlight (natural light) looks like underwater:

Despite that fact in shallow water enough full spectrum light penetrates sufficiently, and the zooxanthellae adapts to the spectrum available, no longer requiring blue light for growth.
See: "The spectral quality of light is a key driver of photosynthesis and photoadaptation in Stylophora pistillata colonies from different depths in the Red Sea" by T. Mass, D. I. Kline, M. Roopin, C. J. Veal, S. Cohen, D. Iluz, O. Levy in the Journal of Experimental Biology 2010 213: 4084-4091; doi: 10.1242/jeb.039891

"Depth zonation on coral reefs is largely driven by the amount of downwelling, photosynthetically active radiation (PAR) that is absorbed by the symbiotic algae (zooxanthellae) of corals. The minimum light requirements of zooxanthellae are related to both the total intensity of downwelling PAR and the spectral quality of the light. Here we used Stylophora pistillata colonies collected from shallow (3 m) and deep (40 m) water; colonies were placed in a respirometer under both ambient PAR irradiance and a filter that only transmits blue light. We found that the colonies exhibited a clear difference in their photosynthetic rates when illuminated under PAR and filtered blue light, with higher photosynthetic performance when deep colonies were exposed to blue light compared with full-spectrum PAR for the same light intensity and duration. By contrast, colonies from shallow water showed the opposite trend, with higher photosynthetic performances under full-spectrum PAR than under filtered blue light. These findings are supported by the absorption spectra of corals, with deeper colonies absorbing higher energy wavelengths than the shallow colonies, with different spectral signatures.".

"Fig. 4. Percent surface irradiance received of different wavelengths at 3 m (grey) and 40 m (black) depth in the waters adjacent to the Interuniversity Institute for Marine Sciences, Eilat, Israel, on 3 April 2008.".

So if you deep dive for your own coral you should be aware that it will thrive under blue light. If you obtain shallow water coral, or buy from the local aquarium supply store, white light is suitable.
Also from: "The spectral quality of light is a key driver of photosynthesis and photoadaptation in Stylophora pistillata colonies from different depths in the Red Sea", (full info above):

"Studies in the Caribbean have found that other corals that are found along a broad depth gradient switch from hosting clade A or B zooxanthellae in shallow water to clade C in deeper water, possibly owing to the ability of the different clades to adapt to different light levels (Rowan and Knowlton, 1995; Baker et al., 1997).".


Do some research on wolves hunting. They certainly have tactics that change depending on the prey that they're hunting, the terrain, danger posed by other members of the prey's herd or family (if any), etc. They're very capable of learning, and use fairly complex communications. They run in packs, live with their mother for a number of years, and have a rather involved family structure that allows for the passing on of behaviors learned from previous generations. It would be difficult to tease out exactly which behaviors are instinctual, and which are learned, but you could say the same of humans as well.


Can someone who is color blind recover color vision by surgical means?

No this is not currently possible as eye replacement surgery is not possible.

Colour blindness is either congenital genetic, such as your X linked forms, or due to a degenerative condition such as retinitis pigmentosa. It can also be acquired through retinal damage or brain injury such as stroke effecting specific areas of the visual cortex.

One of the major problems in restoring colour vision would be that the brain itself may not have the required structure to interpret the signals. The visual cortex is 'patterned' as we develop beginning inside the womb and continuing as a baby. During this process neurological connections in the visual cortex are stimulated so that we develop the necessary networks to interpret the signals from our eyes. If we lack the input of our eyes the brain conducts something called neural pruning where the unused neural connections are destroyed never to be regrown. Therefore if you lack visual stimulus for colour you prune these connections. If we were to somehow replace this colour stimulus later our brains would not be able to interpret it. In a somewhat similar circumstance to this it has been found with individuals who are born with congenital cataracts. If they have their cataracts fixed later in life having spent their childhood blind, despite being able to 'see' they cannot interpret the images they receive.

In individuals who loose there colour due to degenration of the retina, if we were able to repair the retina, through stem cell or transplant therapy then perhaps colour vision would return.

An individual who lost colour vision due to brain injury cannot have their colour vision returned as we cannot repair such injuries.


Is olfactory input processed by the thalamus?

Short answer
Third-order olfactory neurons project to the thalamus and mediate conscious perception of odors.

Background
The human olfactory system is schematically depicted in Fig. 1. The olfactory system is indeed interesting, as it is the only sensory system in which the primary receptor cells project directly to the brain. The olfactory cells in the nasal sensory epithelium project via small, unmyelinated axons via the first cranial nerve to the olfactory bulb in the brain.

In the olfactory bulb, so-called mitral cells project to the olfactory cortex via the olfactory tract. Medial fibers project to the anterior olfactory nucleus and septal areas. Some others cross over to the contralateral olfactory bulb. Lateral fibers contact the primary olfactory cortex.

Now it becomes interesting - third-order neurons in aforementioned regions send projections to the dorsomedial nucleus of the thalamus, the basal forebrain, and the limbic system.

The thalamic connections are thought to mediate conscious perception of odor perception. The amygdala and the entorhinal area are neural components of the limbic system and may be involved in the affective and aversive components of olfaction.

Fig. 1. Olfactory pathway. source: Medscape


When in doubt go back to definitions I say (as I am now).

cytoplasmic determinants: regulatory molecules located in specific distributions around egg cytoplasm

Induction: process by which the presence of one tissue influences the development of others

positional information, signals cells about its relative position to other cells.
hox genes

Differentiation: the process of a cell becoming a specialized type of cell through regulated gene expression

Determination: process by which portions of the genome are selected for expression in different embryonic cells

Pattern formation (aka morphogenesis) → events that determine the spatial organization of an embryo

Hox genes establish anterior posterior axis and regulate gene expression.

I would change,
cytoplasmic determinants → differentiation via determination → pattern formation (rather than information)
morphogen lead to pattern information (since these are the signals)
hox genes → morphogens → pattern information → pattern formation


Does 405 nm light set off phosphorescence in the eye?

Instead of phosphorescence, a more parsimonious explanation is the perception of afterimages. Afterimages regularly appear after viewing a bright stimulus. They occur in the same location in the visual field as the original stimulus, but lack clarity. Afterimages depend on the intensity and contrast of the original stimulus (i.e., they are more pronounced with bright stimuli in a dark environment), the time of fixation (i.e., longer fixation generate more persistent afterimages), and retinal adaptation (i.e., dark environments enhance afterimages).

After images are almost always the complementary color (negative afterimage) to the original stimulus, but can very briefly be the same color (positive afterimage) when viewing an exceptionally bright stimulus. A stimulus consistently produces the same afterimage, which varies in size based on the distance between the person and the background. After images are often revived by blinking.

Afterimages are thought to derive mainly from photobleaching of the retina, although cerebral processes may contribute too.

Phosphorescence in the retina has to be induced by injecting phosphorescent markers (Wanek et al., 2013). As far as I know, the retina is not autophosphorescent.

References
- Gersztenkorn & Lee, Survey Ophthalmol, (2015): 1-35
- Wanek et al., Curr Eye Res (2012); 37(2): 132–137


Do breasts size depend solely on fat amounts?

You are asking two different, but related questions

  Does breast size depend solely on fat amounts?

First, breasts are made up of skin, blood vessels, ducts, fibrous tissue, and fat. There is variation between individuals and within an individual the relative composition changes with age, nutrition, and hormonal status. The size of each of those elements will determine the overall size of the breasts.

  What makes breasts firm or soft given the same size?

We don't know, but it's not fat. You can determine the relative amount of fat in breast tissue (fat is black, or radiolucent, other structures are white, or radio-opaque) using mammography. There is even a term for the ratio of non-fatty structures to fat (mammographic density) but physical findings by trained examiners regarding the firmness or softness of breasts do not correlate with the relative composition of a breast. This is tricky because breast density as it is defined in mammography is relative amount of non-fatty structures compared to fat, but you can't predict the mammographic breast density with physical examination of the breast.


If you are interested in computational neuroscience, I recommend Dayan and Abbott's book: http://www.amazon.com/gp/aw/d/0262541858/ref=redir_mdp_mobile/181-1988504-8834745. This is not a book on neuroscience, not AI, although this particular book has more math than the other introductory neuroscience textbooks I've seen.


Differences between Gradualism and Uniformitarianism

Gradualism is the view that large-scale changes occurs by the accumulated effects of small changes over long periods of time, rather than by rare cataclysmic events of massive effect.

Uniformitarianism is the view that the same forces that shaped the world in the past continue to operate today. Historically, uniformitarianism has often included aspects of gradualism (i.e. definitions by Lyell), e.g. by assuming uniformity of rates. Uniformitarianism was also originally proposed as the opposite of Catastrophism. However, in modern use, the focus lies on uniformity of processes, and rapid catastrophic changes are allowed under uniformitarianism. Also note that the term Actualism is sometimes used for modern interpretations of uniformitarianism.

If we posited that early evolution occurred by small Lamarckian changes and current evolution occurs by small Darwinian changes, we have a model that is gradualist but not uniformitarian.

If we posited that the earth's topography was formed by meteor impacts and massive tsunamis, in sharp sudden strokes of massive effect, but acknowledged that these same processes occur today, we would have a theory that is uniformitarian but not gradualist.

(I don't understand what you are asking in your last paragraph, or how this relates to your main question.)


Do vitamins protect you from common cold?

There are two answers to your question, "emphatically yes" and "sort of."  Vitamins play a critical role in immune function, and a deficiency of certain vitamins can lead to a higher risk of developing an infection.  Specifically, vitamin A, B2, B6, C, D, and E deficiency are linked to depressed immune function.  However that is deficiency, not supplementation above what most people need.

There's a popular idea that megadosing with vitamins, usually vitamin C, lowers the risk or length of common upper respiratory infections (eg the common cold).  The evidence on that is much less convincing.  A metanalysis of studies finds weak or no evidence that it is effective, but may be associated with a small effect.  More study is recommended by the researchers, but they don't go as far as recommending large doses of vitamin C.  (It is also worth noting that large doses of fat soluble vitamins, A, D, E, and K, can be quite toxic and should be avoided).

The magnitude of the first effect is quite large: people with a vitamin deficiency certainly have a depressed immune system.  However it is not clear that larger doses are helpful.


Why do negative ions flow into a cell in an inhibitory synapse, even though a neuron has a negative resting potential?

Short answer
Negative ions can flow against the electrical gradient into the cell, provided their concentration gradient across the cell membrane is large enough.

Background
When an ion channel opens, the resultant ion flow is dependent on two things; the membrane potential (which is indeed negative at rest) and the concentration gradient of the ion.

Consider the activation of a GABAA receptor. GABA is the principial inhibitory neurotransmitter in the nervous system. GABA opens the associated Cl- channel on GABAA receptors.

Using the Nernst equation one can approximate the membrane potential (Veq) at which an ion is in equilibrium. It mainly depends on the concentration of the ion X outside and inside the cell ([X]o and [X]i, respectively).[Cl]o is approximately 103 mM, and [Cl]i 4 mM. Hence, there exists a large concentration gradient with lots of it outside the cell.

Nernst equation. Source: Physiology Web

In a neuron, the Nernst potential of Cl- is around -71 mV. Hence, given that the resting membrane potential is approximately -70 mV for a typical neuron, no Cl- flux will occur when Cl- channels open, because the resting membrane potential is equal to the equilibrium potential of Cl-. However, when a neuron is depolarized by stimulatory neurotransmitters (e.g., glutamate), the membrane potential may be reduced to, say, -60 mV. This is still more negative than the action potential threshold (about -55 mV), but very close to it. So without any inhibition the neuron would be close to firing a spike. However, when GABA is released presynaptically, opening of the Cl- channels coupled to GABAA receptors will result in Cl- influx, because the membrane potential is higher (more positive) than the equilibrium potential of Cl-. In effect, Cl- will enter the cell until its equilibrium potential is reached, re-polarizing the neuron back to -70 mV and hence inhibiting it.


Do neurons that *don't* fire together unwire?

"Specific" unwiring via timing
A more modern understanding of the classic Hebbian aphorism is spike-timing-dependent plasticity. It is observed that connections are strengthened or weakened according to the relative timing of spiking and inputs. Specifically, synapses that are active shortly before a cell fires an action potential tend to be potentiated ("wire"); synapses that are active shortly after a cell fires an action potential tend to be depressed.
So it isn't just that cells that fire together wire together, it's that cells that fire together in a certain way wire together, and cells that fire together in another way "unwire". I think it's important to recognize that a reduction in synaptic strength doesn't necessarily mean immediate loss of a synapse. Weak synapses are common, and only the very weakest are pruned entirely.
Non-specific unwiring via homeostasis
Another general principle, which may be closer to what you are thinking about, is homeostatic plasticity including synaptic scaling. Just like other physiological processes are under homeostatic control, neurons tend to adjust their responses to maintain an overall activity (firing rate) homeostasis. This process occurs on many different time scales and systems, but stated generally, high levels of activity in neurons tend to activate cellular processes that will reduce future activity, and low levels of activity tend to activate processes that will increase future activity.
Current thinking is that synaptic scaling occurs generally rather than specifically. By increasing the strength of specific synapses via Hebbian plasticity and at the same time slightly decreasing the strength of all synapses, the overall balance of input stays about the same (homeostasis).
Of course, things are a bit more complicated when you look over the whole nervous system and the whole time course of development through adulthood, but I think that's outside the scope of this answer.


Is it possible to amplify every single piece of DNA through PCR?

In short; Theoretically yes.

In practicallity no.

Non-specific PCR require random primers to anneal to a target sequence to initiate replication during PCR. Theoretically this should anneal to every combination of bases and therefore allow the amplification of all DNA (or at least in a fragmented form).

Practically, all the primer combinations will have different primer annealling temperatures due to the differential base composition, making the amplification of fragmentation inconsistent, and in others down-right impossible.


Is there a specific terms to describe variant of existing genes in bacteria?

Allele

From wikipedia > allele

  An allele is a variant form of a given gene

I somewhat disagree with this definition in the sense that it is not general enough. An allele is a variant at any locus (locus = position in the genome). You can talk about allele at non-coding sequences. Also, if you are talking about a coding sequence, you can define different sequences as belonging to different alleles whether or not their protein products differ in function or not. The proteins might even be the exact same one for two different alleles if the only difference between these alleles concerns a synonymous mutation (or a mutation in an intron).

You can feel free to define that different sequences as being different alleles by any kind of arbitrary threshold measure. You will just need to define it. For example, you can define that different sequences are different alleles only if they have at least 5% pairwise differences or if you found out by some biophysics computation that they ought to fold differently or for whatever another arbitrary measure.

The term allele is used very often in evolutionary biology and you'll find its usage in any intro course to evolutionary biology.

Rapidly evolving genes

As far as I know, there are no commonly agreed upon definition for what a rapidly evolving gene is. To me, a rapidly evolving gene is simply a coding sequence which evolved more rapidly than other reference sequences. Per se, although it would very likely involve positive selection, I don't think it is a requisite by the definition of rapidly evolving genes. It could, for example, be caused by a very high mutation rate at this particular sequence or by balancing selection causing any new rare alleles to be beneficial.


You can try Velvet, but you'll likely end up with thousands of contigs unless your expected reference genome is pretty simple. This question hits many of the difficulties with de novo assembly. I'm also not sure what you mean by this:

  BTW, in the Geneious I've used a FASTA file for my sequence where my '0' and '1' translated to 'C' and 'D'

Are you trying to use this for a purpose other than actual genome assembly? You say you're from the data security field, so it's unclear what's your end goal. If you only have a binary sequence, you better have a really long read length and hope there aren't too many repeats or you'll really have issues finding a consensus sequence.


Independence of Light independent reaction in photosynthesis?

It turns out that the so-called light independent reactions are not light-independent at all: there are several regulatory mechanisms in place to prevent the turning of the Calvin Cycle when there is no light energy available to produce ATP/NADPH. The hypothetical situation you described in your question demonstrates the necessity of such regulation. The cell cannot allow levels of ATP and NADPH to drop too low because those two factors are required for everything. So if you let the Calvin Cycle run when there is no means of fueling it (ultimately) from light energy, then the Calvin Cycle will run until ATP/NADPH is too low to sustain it further, at which point the cell dies. So several key enzymes in the Calvin cycle are activated indirectly by light.

One of the most well-studied regulatory mechanisms is the ferrodoxin/thioredoxin regulatory system. The enzyme Ferredoxin-Thioredoxin reductase takes electrons from ferredoxin (which is reduced by light energy via the photosystems) and transfers it to thioredoxin, a disulfide-based redox protein. Then thioredoxin reduces several key enzymes in the Calvin Cycle, which activates them (through conformational changes induced by disulfide bonds). The upshot is that when light is around to facilitate reduction, the metabolic enzymes of the Calvin cycle can work, but in the dark the cell oxidizes and these enzymes are turned off, switching off the Calvin cycle and arresting CO$_2$ fixation.

An orthogonal direction of light regulation of the "light-independent" reactions is RuBisCO Activase, which is required to modify the RuBisCO active site to be active. This requires ATP hydrolysis, which amplifies the sensitivity of the Calvin Cycle to ATP availability.

The takeaway is the light-independent reactions may not directly require light as an input, but they are regulated by light availability. I tried to look up how much time in the dark would be required to shift the redox balance such that the Calvin Cycle enzymes would be inactivated, but I couldn't find that data. People in the literature, however, seem to believe it would be quick (1).

There is some description of this at Wikipedia. If you want to look further, Bob Buchanan at Berkeley made a lot of seminal advances in this area; a review of his you might want to check out is (2).

(1): Ruelland E, Miginiac-Maslow M. (1999). Trends in Plant Science. 4(4): 136-141

(2): Buchanan BB. (1980). Annual Review of Plant Physiology. 31:341-374.


Does frequency of eye blinking reveal anything about human biology/nervous system?

People avoid looking at what they don't like thinking about.
A feared enemy, an individual whom you have something to hide from..

Avoidance of looking/excessive blinking is a sign of fear.
It's basically a sign that the individual is not having a good time looking at what he is looking.

Sometimes people are lying and then they don't like looking at whom they are lying to... for them it would be nicer to look out the window or something that takes them away from their subject for a bit of time.
I would expect blinking to increase when lying.

Personally I have noticed excessive durational closing of eyes (a second or so), exactly at the moment of stating their lie.
Those are off course people who are honest to themselves but are trying to be dishonest to you. But some people lie to themselves as well and they may be more difficult to detect.


How do similar environments on islands in close proximity result in allopatric speciation?

The question is a bit confusing because it seems to be built on at least 5 misunderstandings.

Allopatry and gene flow

  [..] allopatric speciation seen in the Galapagos finches. Adaptive radiation occurred because the finches flew from island to island, so there is gene flow [..]

By definition, an allopatric speciation is a case of speciation where there is no gene flow. If there is gene flow, then you may still end up with a reduction of gene flow and a speciation event but that would not be called allopatric speciation.

The first event leading to isolation (that is to an allopatric scenario) might be caused by birds flying over to another island but this does not mean that the divergence between populations occurred with gene flow.

Relative fitness

  [..] the different environments on the different islands provide different selective pressures that causes relative fitness of the same species of birds to change.

It makes little sense to talk about relative fitness of a species. The relative fitness of an individual is the absolute fitness of this individual divided by the absolute fitness of a reference individual (generally a theoretically super fit individual) in the population.

Did you want to talk about competition between species? I don't think so as I don't know how this concept would fit in the rest of the question.

Assumption of similar ecology

  [..] wouldn't it be safe to assume that these islands generally have similar types of plants, similar types of insects, similar climate, similar predators.

No, it really is not a good assumption. In some extreme cases, climate can actually radically differ between two locations at less than 20 meters apart! The same is true for other variable making up the ecological conditions.

Species dependent migration abilities

  If gene flow between populations of finches can occur across islands, why can't it happen for the other biotic factors "contributing" to the islands' characteristics?

Because birds have wings! It is easier for a bird to fly to the next island than it is for a mouse.

Implicit assumption that selection is needed for speciation

  So how can such similar conditions/environments provide selection pressure that is different enough to result in speciation?

Speciation can happen in absence of divergence selection (esp. in allopatry). Genetic drift alone yield to population divergence too and can lead to reproductive isolation.

To my knowledge, the relative role of selection vs drift in causing speciation is not well understood though.


Can low temperatures induce a withdrawal reflex?

The withdrawal reflex is a nociceptive flexor reflex and is a spinal reflex intended to protect the body from damaging stimuli.

In other words, activation of heat receptors is not the trigger of the withdrawal reflex, it is the activation of pain receptors at high, tissue-damaging temperatures.

Extreme cold is also damaging and causes skin lesions akin to heat-induced burn wounds. Again, at a certain tipping point extremeley low temperatures become damaging, and cause frost bites (Sachs et al., 2015). At this point tissue damage will activate pain receptors and these cause the withdrawal reflex to be initiated.

Reference
- Sachs et al., Dtsch Arztebl Intv; 112(44): 741–7


The answer to questions like this is just a guess (Primarily Opinion Based), and I've voted to close. But some food for thought too long for a comment:

  As it is really beneficial for all organisms...

Why do you think that cellulase is so very beneficial to mammals? Animals did have cellulase (some ancient invertebrates still do, like sea squirts, abalone; crayfish have it); we may well have faulty copies of the gene (as @AMR suggested in comments.) But you presume to know we'd be better off with it. That's a belief without any objective evidence.

What might happen if we could convert cellulose into sugar? This is also important to think about. If some of that surfeit glucose in out guts were fermented into alcohol (this condition does rarely occur in humans, and the living people afflicted with this are truly afflicted), because we have a gut microbiome, we would walk around drunk much of the time (ok, maybe even only some of the time), which would make escaping predators less drunk than we were difficult. Maybe the body would be incapable of handling that level of glucose ingestion, and we'd all be T2 diabetics by the time we were just out of toddlerhood.

Humans need fiber in our GI tracts. I don't know all the reasons why we developed that way, but we do. Cellulase would do away with that. Do you know for sure that this would be good for us?

The thing is, you've made an assumption (we'd all be better off with cellulase) that has no evidence to support it at all (or, at least you have not provided any.)

It's always tricky to assume that you know what's more beneficial for a mammal in the presence of billions of mammals that seem to be doing OK. There are millions of reasons that they are doing OK. We don't know all of them, but the absence of the very thing you presume would be a benefit may be what allowed vertebrates to develop at all.

Ancient Origin of Glycosyl Hydrolase Family 9 Cellulase Genes
Structure and function of a cellulase gene in redclaw crayfish, Cherax quadricarinatus


How to get smallest subtree containing a set of nodes from BioPhylo?

The common_ancestor function should give you the result you want: it gives you the tree (I think) that is the most recent common ancestor of all the given targets.


How do ants know where they are going without eyes?

Well, first off, they have eyes, so there's that.

However, a lot of what ants wish to achieve can be done through a combination of a random walk and chemical trails.

When ants are exploring their surroundings, they are essentially wandering about without much in terms of a sense of purpose; laying down a chemical signature as they go.

When they find something interesting, like food, they use their own chemical trail to backtrack, laying down a new chemical trail indicating the nature of what they have discovered, making a kind of smell-road from the hill to the point of interest.

Any ants that subsequently come across this trail follow it, and subsequently join in transporting the food back to the hill.

An interesting implication of this behaviour is the antmill, wherein an ant will lose their trail, and revert to following a nearby ant. If the ant they follow are following them to begin with, this can lead to a spiral of ants that can reach miles in diameter, consisting of confused ants walking until they die from exhaustion.


Why do trees prefer their sunlight a bit diffused?

The studies are very complex and varied. There is evidence that strong omnidirectional light can get through to the understory of dense foliage more effectively.
Here is a Dutch study for crops in dutch greenhouses using light-diffusing rooves which maintain the quantity of light while making it omnidirectional. They report higher growth from diffuse light. https://www.researchgate.net/publication/40803021_The_Effect_of_Diffuse_Light_on_Crops
Studies of tree rings after volcanic eruptions have also found an overall higher growth for the periods following 5 major eruptions.
quotes: Under the presence of clouds, some studies have reported increases in both photosynthetic carbon gain (due to light levels closer to optimal) and water use efficiency, with less impact of photoinhibition due to excessive sunlight (Germino and Smith 2000; Gu et al. 2002)
This research suggests higher growth from direct sunlight in open forests and higher growth in dense, shaded forest under cloudy condition (research)


What are those huge plants / fungi on trees called?

Well I will agree with fileunderwater, it is a Fomes fomentarious. For more info check this: Fomes fomentarius is a tough perennial polypore that usually becomes hoof-shaped with age; it is found on standing and fallen hardwoods. Its woody upper surface develops grayish zones, and its brown pore surface features tiny round pores. When sliced open (no easy task, given its toughness) it is usually composed more of vaguely layered tubes than flesh.

Along with Piptoporus betulinus, Fomes fomentarius is one of two mushrooms that the Tyrolean Iceman was carrying around 5000 years ago. He apparently used Fomes fomentarius as tinder.

Description:

Ecology: Parasitic and saprobic on the wood of hardwoods (especially birches and beech); causing a white rot; growing alone or gregariously; perennial; fairly widely distributed in northern and north-temperate North America

Cap: Up to about 20 cm across; shell-shaped to hoof-shaped; with a dull, woody upper surface that is zoned with gray and brownish gray.

Pore Surface: Brownish; 2-5 round pores per mm; tube layers indistinct, brown, becoming stuffed with whitish material.

Stem: Absent.

Flesh: Brownish, thin, hard.


Computing Percent Identity between DNA / Amino Acid Sequence

tBLASTn, BLASTx and tBLASTx can be used.

It is clearly illustrated here.

If you have just two sequences you need not do a search against the database. You can simply align them using Smith-Waterman or Needleman-Wunsch algorithms, as David mentioned. However, you still need to translate your DNA to protein before doing the alignment. Again, as pointed out by David, with protein alignments you do usually not use identity. Scoring matrices like PAM or BLOSUM are used to calculate similarity.


Do different species of bacteria have distinct absorption bands?

Yes they do, as demonstrated by the fact that bacteria have different colors ! Moreover, some bacteria are photosynthetic and others aren't; the photosynthetic bacteria have a very specific mechanism for absorbing light that the others don't so it stands to reason they won't absorb the same wavelengths.

This page talks about it very nicely, with a list of different colors and bacteria that have them:
http://www.biotecharticles.com/Applications-Article/Colorful-Bacteria-612.html

Money quote :

  Bacteria are pigmented or colored. Pigmented bacteria are also known as chromobacteria. Bacterial pigments are water soluble or insoluble; water soluble pigments are diffused in the growth medium. Chemically, bacterial pigments are pyrrole, phenazine, carotenoid, xanthophylls and quinine or quinone derivatives. The pigment molecules are synthesized in cell wall or periplasmic space. We can visualize pigmentation in bacteria in specific growth medium or my staining bacterial cells with a dye to observe under microscope. It has been proved that only aerobic and facultatively aerobic bacteria are pigmented because, molecular oxygen is essential for pigmentation. Therefore, anaerobic bacteria are nonpigmented. Pigment synthesis is also dependent on light, pH, temperature and media constituents like indicator dyes. They display all the colors from rainbow including light or dark tinges and unual colors like black, white, brown, golden, silver and fluorescent green, yellow or blue.

And the list:

  Purple: Spirillum rubrum
  Violet: Chromobacterium violacein
  Indigo: Janthinobacterium lividum
  Blue: Streptomyces coelicolor
  Green: Chlorobium tepium
  Yellow: Xanthomonas campestris
  Orange: Sarcina aurentiaca
  Red: Serratia marcenscens
  Brown: Rhizobium etli
  Black: Prevotela melaninogenica
  Golden: Staphylococcus aureus
  Silver: Actinomyces sp.
  White: Staphylococcus epidermidis
  Cream: Proteus vulgaris
  Pink: Micrococcus roseus
  Maroon: Rugamonas rubra
  Fluorescent blue/green: Pseudomonas aeruginosa
  Fluorescent yellow: Pseudomonas fluorescens

It appears some purposes of producing pigments, aside from photosynthesis, are to absorb UV light (i.e. absorbing a specific wavelength is the entire point) or mopping up free radicals.

An additional note, from the Wikipedia page for Rhodospirillum rubrum, the first bacterium in that list (which Wikipedia describes as "pink" but close enough):

  The photosynthesis of R. rubrum differs from that of plants as it possesses not chlorophyll a, but bacteriochlorophylls. While bacteriochlorophyll an absorbs light having a maximum wavelength of 800 to 925 nm, chlorophyll absorbs light having a maximum wavelength of 660 to 680 nm.

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

And while that paragraph describes "chlorophyll a" as being a feature of plants, other bacteria do use it such as Chlorobium tepidum, so there you can see some wavelengths that are absorbed by one and not the other.


Why estimate linear and full (linear, quadratic, and correlational) selection coefficients separately?

This is directly following the advice of Lande & Arnold (1983), saying:

  Linear multiple
  regression can be used first to estimate the forces of directional selection, $\beta$, and their standard errors. Then a quadratic multiple regression (16) or (Al), can be used to estimate the forces of stabilizing selection, $\gamma$, with their standard errors. The regression (16) provides the best quadratic approximation to the selective surface (although valid estimates of $\beta$ can be obtained
  only from a purely linear regression, or by using the orthogonal regression (Al)).

The reason is that the estimates of direction selection is influenced by the higher order terms in the full model that includes quadratic and correlational selection, and the linear model therefore has the best estimates of the change in mean value over a generation of selection ($s = \bar{z}_{after} - \bar{z}_{before}$). However, the full model is the better representation of the fitness surface. There are also other methods to approximate the fitness surface.

For the record, I used the same approach in my master's thesis many years ago.


Effects of Polyphasic vs Monophasic sleep in humans

Reading "Polyphasic Sleep: Facts and Myths (Dr Piotr Wozniak)", it is pointed out that infant humans do undergo polyphasic sleep. As this is where most of our development is obviously done, I do not know where I can further proceed with the question about how it would affect development?  Perhaps the issue is more how it would effect the day to day performance of a developed individual?  If this is the case then it is suggested by Dr Wozniak that this is likely to be highly disruptive to the individual

Those well-defined effects of natural sleep affecting stimuli on sleep patterns lead to an instant conclusion: the claim that humans can adapt to any sleeping pattern is false. A sudden shift in the schedule, as in shift work, may lead to a catastrophic disruption of sleep control mechanisms. 25% of North American population may work in variants of shift schedule. Many shift workers never adapt to shifts in sleep patterns. At times, they work partly in conditions of harmful disconnect from their body clock, and return to restful sleep once their shift returns to their preferred timing. At worst, the constant shift of the working hours results in a loss of synchrony between various physiological variables and the worker never gets any quality sleep. This propels an individual on a straight path to a volley of health problems...
It appears that polyphasic sleep encounters the precisely same problems as seen in jet lag or shift-work. Human body clock is not adapted to sleeping in patterns other than monophasic or biphasic sleep.

It would therefore seem that polyphasic sleep is certainly detrimental to health, if not development.
However studies into cognitive performance resulting from differing sleep patterns run by Dr Claudio Stampi (Published ISBN 0-8176-3462-2), he concluded that polyphasic sleep was more efficient than monophasic sleep.  Therefore it may be possible that polyphasic sleep patterns have no detrimental effect on development.

Individuals sleeping for 30 minutes every four hours, for a daily total of only 3 hours of sleep, performed better and were more alert, compared to when they had 3 hours of uninterrupted sleep

There are a couple of theories mentioned in the above book (beginning pg 5) which support the development of monophasic sleep as evolution rather than a social convention:

Polyphasic sleep is regularly seen in smaller mammals that have very high metabolic rates, requiring them to spend most of their time foraging or hunting.  Therefore a long sleep would be highly impractical for them as they would wake without the energy required to hunt their next meal. Humans do not have this need as they are larger and do not require such regular meals.
Monophasic sleep would be beneficial for the early human hunter gatherer as our eyes are not well adapted to see at night.  Therefore any time spent not using the daylight is wasted and any time without the light is not nearly as useful.  This makes it more beneficial to sleep for an extended period when the sun is down.

I am sure that social factors would have an effect, however I would imagine the evolutionary pressures to be more significant.
I really would recommend the book (http://sleepwarrior.com/Claudio_Stampi_-_Why_We_Nap.pdf) if you have not yet encountered it as I found it very informative and packed with references to studies that you may find helpful.


Why is the internal capsule dark in this transverse section of the brain?

Short answer
White matter is called white matter because it is relatively white compared to gray matter. However, in fixated specimens it is not as snowy white as in textbook pictures.

Background
The internal capsule is a paired V-shaped structure that is visible in horizontal brain slices (Fig. 1). It is a subcortical structure mainly consisting of fiber tracts connecting the cortex to the brainstem.

Fig. 1. Horizontal (transverse) brain slice showing internal capsule. source: Utah University

In Fig. 1 the structure is quite white'ish, but in the following two images you can see it is not always the case.

source: The Human Brain: Chapter 5: The Cerebral Hemispheres

Fig. 3. source: Medicos Notes

As you can see, the internal capsule is not always nice and white. Fig. 2 particularly shows a reddish taint of many white matter structures.

The internal capsule is well-vascularized (Schamann, 2003) and strokes in this region are associated with muscle weakness and loss in sensory sensitivity (source: Stanford Medicine). Hence, the red coloration may well be due to red blood cells that have not been completely washed out of the brain beore it was fixated. Also, non-specific coloring may happen over time in fixated specimens and many fixation artifacts can occur that lead to alterations in gross morphology (Chatterjee, 2014).

References
- Chatterjee, J Oral Maxillofac Pathol (2014); 18(S1): S111–6
- Schamann, Stroke (2003); 34: 2264-78


Why didn't humans evolve to reproduce identical twins all the time?

What you describe could have happened under the right conditions. However, there are a few things you haven't considered.

Because humans are especially altricial, always having twins would double the cost of children on parents.
The benefit of sexual reproduction is immune diversity. So a population like this could be far more vulnerable to disease.

So as far as this thought experiment goes, genes can't be too selfish or they dramatically reduce their own fitness. It's something worth simulating computationally to see what happens.

References

Sexual reproduction as an adaptation to resist parasites (a review)


What is the meaning and significance of extreme pathways

For any dynamic system defined by different components, the steady state is the state of the system in which the components remain constant over time. If you consider the example of growth (by cell division) the point at which the total number of cells remain constant would be the steady state. This is a point at which birth rate = death rate. Similarly for a multi-component system such as a gene and its activator, the steady state would be the point where the mRNAs and the proteins of the gene and its activator are constant. If only few components are constant then the system is said to be in a quasi-steady state.

A point to be noted that in chemical (or biochemical) systems steady state, as a term, is different from equilibrium (in physics these terms are used interchangeably). Equilibrium is a condition when, for a single reversible reaction, the forward rate = backward rate.

In mathematical terms steady state is a point where the rate of change of components = 0. In an ordinary differential equations based model:

$$\frac{d\bar{X}}{dt}=0 \\$$
where $\bar{X}$ is a vector in which each element is a component of the system. In case of the transcription example, $X(1),X(2)..$ would be mRNA, protein, activator mRNA and so on. In other words $\dfrac{dX(i)}{dt}=0$ for all $i$.

Steady state capabilities should mean the properties of the system at its steady state.

The kind of study described in the question is called metabolic flux balance analysis in which different metabolic reactions are described in the form of linear equations represented by $Sv=0$ where $v$ is the vector of all fluxes (metabolic reaction rates) $S$ is the stoichiometry matrix (which has the stoichiometry of all components in different metabolic reactions). The RHS is zero because we are evaluating the system at its steady state i.e. we are interested in finding out the condition in which the net metabolic reaction flux is 0. In other words all metabolic reactions, balance each other.

You need to read more about this. There are a lot of books on this topic. You can start with this review.

In flux balance analysis, the linear equations are overdetermined i.e. there are many solutions. People generally use linear programming (simplex algorithm) to find optimal solutions. In the space of the optimal solutions, the vertices represent extreme reactions. The entire optimal solution space can be described as a linear combination of these extreme reactions.

  Schematic representation of a convex cone characterized by five
  extreme pathways. Extreme Pathways 1–5 (EP1, EP2, EP3, EP4, and EP5)
  circumscribe the solution space for the three fluxes indicated (vA,
  vB, vC). EP4 lies in the plane formed by fluxes vA and vB.
  Consequently, flux vC does not participate in that extreme pathway.
  EP3, EP4, and EP5 are all close and represent different uses of a
  network to achieve a similar overall result. All points within the
  convex cone can be described as a non-negative linear combination of
  the extreme pathways [1].


Using RNA-seq to compare gene expression across patients instead of between Control and Experimental conditions

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

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

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

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

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


How do rodenticides with delayed effect work?

These poisons prevent recirculation of vitamin K and thus formation of prothrombin which is essential for coagulation of blood and are required for maintaining the integrity of capillaries. The depletion of vitamin K is slow and in a couple of days internal hemorrhage occurs extensively and the animal dies of shock. Early recognition of poisoning in humans and other animals can easily be treated with administration of vitamin K.
http://en.m.wikipedia.org/wiki/Rodenticide


Why is there a layer of moist lining the inner walls of alveoli?

The fluid in the alveoli contains phospholipoproteins that act as pulmonary surfactant, which keeps the alveoli open during breathing.


How much does 10g of glucose raise the blood glucose level?

If you get an intravenous injection containing 10 g of glucose, all glucose will enter the blood within few seconds and your blood glucose level will temporary rise by ~200 mg/dL.

If you take 10 g of glucose by mouth, the glucose will be dissolved and distributed within the stomach and small intestine and will be gradually absorbed into the blood, let's say within 30 minutes. In this time, some glucose will already move from the blood into the cells, so you will never have 10 g of additional glucose in the blood at a given time.

The actual blood glucose rise after ingestion of 10 g of glucose is not a fixed number, but a range that depends on several factors:

  The gastrointestinal tract plays a major role in the regulation of
  postprandial glucose profiles. Gastric emptying is a highly regulated
  process, which normally ensures a limited and fairly constant delivery
  of nutrients and glucose to the proximal gut. The subsequent digestion
  and absorption of nutrients are associated with the release of a set
  of hormones that feeds back to regulate subsequent gastric emptying
  and regulates the release of insulin, resulting in downregulation of
  hepatic glucose production and deposition of glucose in
  insulin-sensitive tissues. These remarkable mechanisms normally keep
  postprandial glucose excursions low, regardless of the load of glucose
  ingested.** (Role of Gut in Glucose Homeostasis, Diabete Care, 2016)


Welcome to Biology.SE!

Your question is very broad. Also, your post has the default of containing severals questions in it. Make sure in the future to restrict your post to only question, it will be much more likely that you receive a good answer then. I hope that I can give some indications about how to get some more knowledge in this answer. In this answer, I do not consider all your questions one by one to answer them (or guide you to the answer) but I think that all your questions will get an answer as you learn more about the subjects I cite. Hope that answer will help you.

Very basics of molecular genetics

You should start to have a few ideas about genetics. Make sure you know what is a chromosome, a gene, an allele, a protein and a phenotype. Wikipedia will help you with that. Come back on Biology.SE if something seems unclear to you.

Basics of genetics and evolution

You are definitely interested in concept of segregation. This is a very fundamental concept in genetics. The basis of the laws governing segregation has been first discovered by Gregor Mendel and we still name these basics laws after Mendel. We talk about Mendelian segregation. You may want to google that.

Then you are interested in the concept of heritability. I have been talking about heritability in different posts. In the third sentence of my answer here, there is a short list of posts that define the concept of heritability.

Eye color you said?

You talked about the genetics of eye color inheritance. Here is a post that will interest you then.

The Genetics of Development

Your question is not only about genetics but is about the genetic of development. You may want to have a look to the basics of developmental biology. The most famous DNA sequence  involved in determining the body plan of many different living things are the so-called homeobox. There is plenty of interested things about this homeobox. This post may interest you btw.

Rough details about the evolution of development along the tree of life

  How come that information [architectural information] is not changed in thousands of years or even millions of years?

It really depends on what you call architectural information. But in any case it does evolve. If you think of things such as like size of an animal. Then it may evolve fairly quickly. You may thing of more important change, such as evolving a new pair of legs or evolving wings or a head, then it tends to take more time. Below are just a bunch of examples of how animals differ in terms of body plan along the tree of life.

You might be interested to study a bit the development or early animals. Some have a radial symmetry while other (like us) have bilateral symmetry (see wiki). Some animals have a head, some don't. Some animals have two dermes while others have three dermes. The Deuterostomata (vertebrates, tunicates, echinodermes, ...) have a development where the blastopore of the gastrula becomes the anus while in the protestomata (now thought to not be monophyletic and divided into ecdysozoa and lophotrocozoa (see here)) the blastopore becomes the mouth. Among the arthropoda (insects, spiders, millipedes, ...) the story is very interesting as well. Some have a highly segmented body with a pair of legs at each segment (millipedes) while other groups have fused those segments. Spiders have only two big body parts, while insects have three big body parts. In insects, the thorax (one of the 3 body parts with the head and the abdomen) contain three segments and each segment hold a pair of legs. The first flying insects also had three pairs of wings, now degenerated into two and even into one in Diptera.


In humans what is the last metabolic process to cease after death?

My answer isn't researched; it is speculative.

I interpret metabolic processes as anabolic or catabolic processes. I assert that only anaerobic processes can continue for a long time after vegetative death (the epithelia could house a counter-example of a post-mortem process, but I can't think of one), and I speculate that only catabolic processes are likely to have sufficient pools of reactants to continue after death. So we're looking for a catabolic process with a large reactant pool. Therefore I think that the action of digestive proteases will continue for the longest time, because these enzymes are very stable and could have a lot of substrate around (including, at a very slow rate, cleaving each other.) The neutralization of stomach pH would inactivate this process...I don't know how long that takes.

If something like blood clotting is considered a metabolic process, then probably that continues the longest. The binding of CO₂ by hemaglobin is probably faster than blood clotting. Again, I don't really consider those processes to be metabolic.


If it were me...

You can resuspend the two separate pellets (A and B) in 10ul each.
Collate in one tube (add A to B).
Use the remaining 10ul  from your desired volume to 'wash out' tube B and add the wash to tube A.

So long as the DNA is from the same sample this is a perfectly reasonable step that should not result in a substantial loss.


How many co-expressed genes would be expected in a tissue?

Check the beautiful publication of Daniel Ramsköld et al. 2009, which holds the numbers for generally anticipated co-expression.
The specific level of co-expression, which applies to your scenario, will depend upon your tissue, your thresholds, and your definition of co-expression.
It you look for a co-change of some genes across different specimen (rather than co-expression), the number of genes that should change will depend upon the underlying biology (and thus prevent a general answer without considering the specifics of your specimen).


Homework question on chemically defined medium

A chemically defined medium is, according to this Wikipedia article:

  ... a growth medium suitable for the in vitro cell culture of human or
  animal cells in which all of the chemical components are known.

Four of the five components fit this criterion precisely, as they are chemical formulae (and of course a common name for a compound whose formula is well known).

However, even though you know exactly how much yeast extract was added to the medium, you do not know its exact chemical composition. To be sure, assays of the chemical composition of yeast extract have been run, and one could come up with approximations of it's makeup. But the bottom line is that there is no precise chemical formula for yeast extract as there are for the other components of the medium.


Could murder be modeled as an infectious disease?

Disclaimer: I'm an infectious disease modeler, and generally pretty skeptical of "We modeled X like an outbreak!" claims, because many are just an exercise in curve fitting.

Given that, the answer is both "Yes" and "No".

"No": Murder as an act really isn't transmissible, and if its not transmissible, it can't be modeled as an infectious disease.

"Yes": It is probably possible to model some things in the same way we model infectious diseases, because the underlying causes of murder may be somewhat 'transmissible'. Certain behaviors, cascading effects (if one family member is incarcerated it increases the likelihood that other members of that family will be incarcerated) etc. might give crime "disease-like" properties.

That's probably largely driven by underlying social networks and the like, which are also important to infectious diseases. But then you have a problem in reasoning. For example, did murder "spread" along a social network, or did we merely sample a group of people with a shared underlying cause (for example, poverty, membership in gangs, etc.)

It's probably useful to model some of these things, but it's more useful, in my mind, to model them as their own process, rather than trying to shoehorn them into being like a disease.


Sexual selection in cats or other animals

Wilson and Reeder (Mammal Species of the World) count 40 species of Felidae. Most of them are small cats (subfamily Felinae). Lions are in the subfamily Pantherinae, which contains only 6 species, one of them the jaguar, Panthera onca, which is solitary, like the tiger, Panthera tigris. By what I know of small cats, Puma concolor included, and the tiger and the jaguar, it seems that lion social behavior is not typical of felines. (Would add that as a comment, but can't comment with reputation < 50).

EDIT:

Looking for "Felidae sexual selection" or 'Felidae "sexual selection"' in google I have found some links. Look for "sexual selection" or "Felidae" in the text. Though I'm afraid most of them are not exactly what you're looking for, maybe they can open new windows of thought. Hope that helps!

http://www.journals.elsevierhealth.com/periodicals/aaeth/article/0304-3762%2883%2990116-5/

http://www.catsg.org/cheetah/05_library/5_3_publications/E/Eaton_-_The_Evolution_of_Sociality_in_the_Felidae.pdf

http://onlinelibrary.wiley.com/doi/10.1111/j.1095-8312.2010.01520.x/pdf

http://www.jstor.org/discover/10.2307/3544917?uid=26584&uid=3737664&uid=5909624&uid=2&uid=26582&uid=3&uid=67&uid=62&sid=21103320511793

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

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0048352?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+plosone%2FPLoSONE+%28PLOS+ONE+Alerts%3A+New+Articles%29

http://books.google.com.br/books?id=FhvmHW972mAC&pg=PA752&lpg=PA752&dq=Felidae+%22sexual+selection%22&source=bl&ots=Ns8iRUQxXW&sig=r5ZEgp-nH9mll5cYgB5GzNaThZs&hl=en&sa=X&ei=FBPQUq63LPDLsQS0m4DAAw&ved=0CDYQ6AEwADgK#v=onepage&q=Felidae%20%22sexual%20selection%22&f=false

http://www.mapoflife.org/topics/topic_203_Baculum-%28penile-bone%29-in-mammals/

http://www.sciencedirect.com/science/article/pii/S0169534703003999


Are nutrients absorbed in human esophagus?

For several reasons, I seriously doubt that this has been studied extensively.

There is a good reason to study absorption through oral mucosa because a drug or glucose can be held there by people who needing rapid absorption of a drug (e.g. sublingual nitroglycerine) or by people who may be unable to swallow (e.g. a hypoglycemic individual who has lost consciousness). Where there is a reason to know, there is a reason to study something.

The esophagus, on the other hand, is normally an area of rapid transport (a pill, or a fluid, for instance, is in the esophagus less than 10 seconds). While it's assumed that some pregastric absorption through the esophagus occurs and might be beneficial to avoid a "first pass" metabolism of the drug by the liver, there is no good method to keep a drug in the esophagus. With that in mind, absorption from the sublingual mucosa (where a pill might be held) is more valuable than what might get absorbed in as little as 6 seconds in transit to the stomach. From that point, it will spend significant amounts of time in the stomach, the various sections of the small intestine, and the large intestine.

Absorption of drugs from the rectum has been studied, because it can be used, once again, as a method of drug delivery when another route for whatever reason cannot,

Esophageal motility disorders occur, so studies of esophageal function are common. But as the esophagus is never normally the place for absorption of nutrients, there is no reason to study it except for the sake of satisfying pure curiosity. Studies take time, involve volunteers (or paid recipients), risk, and money. Pure curiosity is a reason to study something. But to get the all the previously mentioned factors to come together and fund a study, the reason usually outweighs pure curiosity.

Esophageal scintigraphy: reproducibility and normal ranges
Oesophageal transit of a radionuclide solid bolus in normals
DRUG ABSORPTION BY SUBLINGUAL AND RECTAL ROUTES


What insect is this? I saw it in my house in Kolkata on 2 April 2018, at 8:00 p.m

I would concur with user22542 --> order Diptera: family Dolichopodidae

Supporting evidence outside of wikipedia is on an Australian website. http://www.bowerbird.org.au/observations/35021

I don't suggest them to be the same species, however potentially related as they seem to live in grassy places across the globe.


How do chromosome pairs get "paired up" for protein synthesis?

Although we think of these as coming in pairs, are they actually attached or paired up in some way?

Chromosomes only pair up during metaphase I of meiosis. And meiosis only occurs during the production of gametes (sperm and oocytes). Say Chr1 from mom pairs up with Chr1 from dad. http://media.web.britannica.com/eb-media/76/94976-004-7D0416E7.gif

Mitosis is what happens when somatic cells (say in your toes) replicate.  Chromosome (inherited from your mom and dad) do not pair up in mitosis. Instead each chromosome is replicated

You are probably confusing chromosomes pairs (one copy from mom and another from dad) sitting side by side... undergoing chromatid crossover... with sister chromatids (ie the same chromosome which has been duplicated, so each daughter cell can have its own copy.) This forms the X shape that you think off when imagining a chromosome.

Transcription occurs on all 46 chromosomes. Aside from situations where the gene is controlled by parental epigenetics... both the paternal and maternal copy of the gene is active.

As for  recessive/dominant allele... it has more to do with the function of the protein. If the protein is produced by one allele in sufficient to give a normal phenotype, then the allele is dominant. A dominant negative tends to occur when the mutant allele codes for a mutant protein that can interfere with the normal function of the protein that is encoded. A common example is that the protein works as a pair. And is one member of that pair is mutated, the entire complex is non-functional.


Why do we add salt when precipitating DNA?

The role of the salt is to neutralize the charge of the DNA's sugar phosphate backbone.  This makes the DNA less hydrophilic (less soluble in water).

Ethanol has a lower dielectric constant than water so it's used to promote ionic bonds between the Na+ (from the salt) and the PO3- (from the DNA backbone) causing the DNA to precipitate.


Text Book Recommendation: Cell & Molecular Biology + Organic Chemistry

Given your requirements I would go for the Alberts for molecular cell biology.

For organic chemistry, in my opinion, there is no better book then the Clayden. It is targeted at OC students but I - as a biologist - learned a lot from it and still sometimes love to browse through it even though my work is far away from organic chemistry.

In general, I would advise you to go to your local library and take a look at the different choices before getting one. Take your time to get a feel for the writing and teaching styles and pick the one you find most access to (and maybe give feedback as a comment/an own answer to your post which book you took and why, for future reference).


How does the human stomach handle a mix of digested and undigested food?

The regulation of emptying of food from the stomach to the duodenum takes place with the help of feedback mechanisms involving the duodenum and stomach.

Nature of the chyme which inhibits stomach emptying by the duodenum:

Excessive acidic chyme.
Chyme contains too much undigested or unprocessed proteins and fats due to which its tonicity and irritability changes.

Regulation by the duodenum:

Nervous regulation:
The enteric nervous system,the vagus and the prevertebral sympathetic ganglia play the key roles in nervous regulation of this feedback mechanism because when food enters the duodenum they provide stimuli that activates them which inturn inhibits pyloric pump.
Hormonal regulation:
Cholecystokinin, secretin and gastric inhibitory peptide inhibits pyloric pump,gastric motility,gastrin effect on stomach emptying respectively.

Thus,when much undigested chyme passes to the duodenum,duodenum regulates if the digestion process should be prolonged or not in the stomach.

Factors promoting emptying of stomach:

Gastric food volume and gastrin hormone promotes emptying by stimulating the enteric nervous system for emptying and enhancing pyloric pump respectively.

Thus, the distinguish between a digested or undigested chyme to be passed to the duodenum or the time for which the food must stay in the stomach for digestion is entirely under the regulation of these factors.

References:

https://www.ncbi.nlm.nih.gov/pubmed/1126597

https://www.ncbi.nlm.nih.gov/pubmed/7943335

https://en.m.wikipedia.org/wiki/Gastrin


There are plenty of animals with brief procreative periods, as you suggest. In chimps, sex takes 10 to 15 seconds - much less time than humans. So the question is really why have humans evolved to be different?

I don't think any of the answers based on fitness are particularly compelling. It's not like sex feels like running a marathon or less physically fit people can't manage to ejaculate in their partners so it seems unlikely that the lengthy sex act serves to distinguish fitter individuals.

Instead, I think the difference probably lies in the pair-bonding role of sexual activity. Humans form unusually long-lasting, typically monogamous or largely monogamous, bonds that function to provide the support needed during the lengthy childhood that humans undergo. The prolonged, and highly pleasurable, sex act likely functions to help maintain these bonds in order to keep the couple together and provide the stable support needed to maximise the chances of successfully raising a child to adulthood.

Unfortunately, to the best of my knowledge, there is no high quality empirical evidence that would convincingly answer the question so any answer must be somewhat speculative.


Retrieve the associated annotation from Uniprot

You can upload your list of accession numbers to the batch retrieval service for the UniProt Konwledgebase, http://www.uniprot.org/uploadlists

A video tutorial for this service is available at https://www.youtube.com/watch?v=kLdgjqWoMZc

Once you have retrieved your proteins, you can click on "Columns" to customize your output and add columns, e.g. for function annotation. See also http://www.uniprot.org/help/customize or http://insideuniprot.blogspot.ch/2015_03_01_archive.html
Results can then be downloaded in tab-separated format.

If you have any additional questions, please don't hesitate to contact the UniProt helpdesk.


What is this plant with distinctive leaves?

Seedlings are often tricky to determine, but I think this may be the common weed Chenopodium album (from the family Amaranthaceae). This is common across Europe, and the leaf shape, growth pattern and the silverly underside seen on the top leaf in your picture fits well.

Here are pictures of a seeding and a larger plant:

(from flickr.com)

(from https://plants.ces.ncsu.edu)


How can there not be purpose movement in the fetus until week 18, when a fetus can open its mouth and suck its fingers at week 11?

Swallowing (Nishino, 2013) and sucking (rooting reflex) are reflexes. The fingers may just happen to be in the vicinity of its oral region (they often are; Fig. 1.), and oh boy are babies keen to grab a nipple when it's close! Mouth openings can henceforth be also reflexive, being part of the rooting reflex.

Fig. 1. Fetal hands in facial area. sourceL: ABC News

Reference
- Nishino, Front Physiol (2012); 3: 4892013


Why isn't the ovum reabsorbed into the body (like sperms) if it is not fertilised?

Apparently they are
Technically speaking, the ovum is not shed because it does not exist unless and until fertilization occurs.  Development leading up to the ovum otherwise stops before the final division of meiosis.
Now, you can ask why the body doesn't reabsorb oocytes, but then the answer is that it does, in a process called follicular atresia, with one or a few exceptions per  month.
Now what about that secondary oocyte that isn't fertilized?  Well, it's time to pull out a lovely article from 1917 (Harry Carleton).  Why are we so unable to match such prose today?  The paper describes a mouse study, giving quite recognizable descriptions of membrane blebbing and nuclear fragmentation characteristic of apoptosis in a decade during which it is usually said to have been forgotten.  (A 2005 work reports this for unfertilized human oocytes) Carleton likens the apoptotic changes he observed to atresia in the ovary, and says that the oocytes are reabsorbed by phagocytic cells.


Can cancer cells in the same person, organ, and origin have different DNA?

Cancer cells and normal cells differ on the genetic basis but they share the same genetic background, so they have not different DNA in the sense of two different people. They have to be different, since cancer cells have to accumulate mutations on a number of genes to become a cancer cell, which can survive and will not be directed into apoptosis. These are genes which control the cell cycle, certain growth factors, tumor suppressor genes, cell signalling and so on. In all these genes there need to be either activating or deactivating mutations present. Most of these mutations are point mutations (single nucleotide polymorphisms, SNP), where only one base is altered to achieve a mutation. An example for such a mutation would be the mutation in the B-RAF kinase, which is involved in signaling and activating genes, where a point mutation exchanges Valine 600 to glutamic acid (V600E, for reference see here). These are relatively small differences between these two cells. The Cancer Genome Project aims to sequence cells from a cancer and also normal cells from the same individual and then do a comparison. Later stages tumors often tend to genetic instabilities where complete regions of the genome are duplicated, inverted or deleted, see here for a review.
A more basic overview is given by the Ebook "Essentials of Cell Biology" by the Nature Group, which has an overview of cancer cells.

Regarding the mutation rate, this is hard to estimate. There are a few papers available here, but they focus on the mutation rate in germ cells, so these are mutations that are transmitted to the next generation. The estimates there are between 70 and 100 mutations per generation per individual, depending on the research method. You can find a nicely explained blog article here, which gives a number of original references, too.

The mutation rate in cancer is a different thing, since this depends on which genes are mutated. The mutation rate for cancer has to be higher for the cancer cells to allow to collect the necessary transformations into a cancer cell, but these mutations seem to occur only in a few hotspot regions of the genome (Further references can be found in this article called "The causes and consequences of genetic heterogeneity in cancer evolution" and in this called "Emerging patterns of somatic mutations in cancer"). There are two article called "The mutation rate and cancer" which are interesting in this context. They can be found here and here. As always, if you have problems with getting the articles, let me know, I can help there.


What does "cellular" mean in this context?

My understanding is that the slime in question is formed of the bodies (the cells) of the dead diatoms. Where does porous come into it? Is it mentioned in a previous sentence?


No analogues of the CRISPR-Cas system have been found in any eukaryotic species, including humans. So far, it appears to have evolved only in prokaryotes and archaea.

Reference: Evolution of RNA- and DNA-guided antivirus defense systems in prokaryotes and eukaryotes: common ancestry vs convergence


What does FETCO2(end-tidal fraction CO2 concentration) represent?

I'm not sure if you're asking about the procedure or the underlying concepts of CO2 concentration or how a capnometer works.  But in brief, it is measured at the end of an exhaled breath, which is least 'contaminated' by inhaled but unused air from the conduction zone (trachea, etc.).  The measurement is done by looking at the blockage of light from an infrared light to a sensor by the CO2 - exactly the same mechanism by which global warming works.  And the way it's reported is, in this case, as a fraction from 0 to 1.  It could be reported as a percentage by multiplying by 100, or as a partial pressure by multiplying by the total atmospheric pressure (often 760 torr at sea level).


Know your databases! This is just the query fit for OMIM.

http://omim.org/entry/206500

  Anencephaly is considered an extreme form of neural tube defect
  (182940), which has been associated with variation in several genes.
  The entity described here is believed to show autosomal recessive
  inheritance.

The genes are those associated with neural tube effects, i.e., VANGL1, T, CCL1, and FUZ. See also folate-sensitive neural tube defects.

http://omim.org/entry/182940

The folate evidence was so convincing that the US/Canada in the 1990s introduced folate supplementation in all bread, flour, and cereal products. Today, US/Canada have a lower incidence of NTD (neural tube defects) than Europe, where folate supplementation is completely left to one's choice (and if women actually care they take it too late).


How do biologists quantify "gene expression" in experiments?

The primary product of protein coding genes are mRNAs.  When we talk about measuring gene expression we want to assay the steady-state levels of a specific mRNA within a cell.  This is usually accomplished by starting with a large number of cells and harvesting all of the mRNAs from all of the cells.  One way to measure the expression level of just one gene's mRNA is to perform a Northern Blot.  Other sensitive methods include: an S1 nuclease protection assay, an RNAse protection assay, and a primer extension assay.

Microarrays have also been used extensively to measure expression levels of thousands of genes at the same time in a single experiment.

With the advent of RNA-Seq methodology it is possible to count the number of transcripts in an experiment (if you have a sequenced reference genome)


What is the difference between a phosphotransferase, a phosphatase, a phosphorylase and a kinase?

Don't get caught in the linguistic trap of attaching too much significance to the precise meaning of any one piece of scientific jargon. Nomenclature, the system of naming things, utterly sucks in biology, and it sucks even harder for protein biology. There is no one universally accepted classification and naming system for proteins, although there have been plenty of attempts.

For example, phosphotransferases are classified as EC number 2.7. However, Glycogen Phosphorylase is classed under 2.4, which might make you think "well, clearly kinases are enzymes that transfer phosphate groups from organic substrates such as ATP and are classed as 2.7, whereas phosphorylases are enzymes that transfer from inorganic substrates and are therefore classed as 2.4". But wait! RNase PH is a phosphorylase that's classed under 2.7 and uses inorganic phosphate, so um... yeah.

In any case, don't get too hung up on the nomenclature. Unless you're working in an enzymology lab just say "kinase" and everyone will know what you're talking about.


Do we know of any "species ending bugs"?

From the vantage point of other species, humans might be considered "bugs" in the sense that we are organisms that are causal in the ongoing extinction of numerous species. We're doing a pretty good job of it, so far:

  The included extinctions span numerous families of plants[4] and animals, including mammals, birds, amphibians, reptiles and arthropods. With widespread degradation of highly biodiverse habitats such as coral reefs and rainforests, as well as other areas, the vast majority of these extinctions are thought to be undocumented, as the species are undiscovered at the time of their extinction, or no one has yet discovered their extinction.   The current rate of extinction of species is estimated at 100 to 1,000 times higher than natural background rates.


Predicting DNA nucleotide bases sequence from fully formed protein

It's trivial in principle, but remember that there are multiple codons that can produce a single amino acid, so reverse-translating a protein will either give you the most commonly-used codons for the protein, or will give you a large number of possible sequences.

Here and here are online programs that will give a single consensus, and here is one that considers ambiguities.


Why do some viruses cease being a problem even though no vaccine or cure is found?

Infections spread in a population when the number of new infections caused by an infected person is greater than or equal to 1.

If each infected person spreads the virus to less than 1 person, eventually no one will be infected, without a need for any sort of cure. Of course, the longer a deadly infectious disease spreads in a population, the more people will die during this process. Ideally you want to get the number of transmissions as close to zero as possible as quickly as possible.

SARS and MERS are each a bit different, but share some similar characteristics. Compared to COVID-19 caused by SARS-CoV-2, both are more severe in a larger fraction of the people infected (note: all three viruses are closely related betacoronaviruses). This made it easier for public health officials to identify and isolate infected individuals.

The MERS virus is really not gone at all: it lives on in animal reservoirs, like camels (so it is primarily only a concern in places where those reservoirs live). Cases continue to occur sporadically. However, MERS is usually not that transmissible between people, having a natural transmission rate that is already less than 1: that means that most people who get it get it directly from an animal, and don't continue to spread it to others besides occasional infection of individuals with close-contact, like a family member. There have been exceptions where isolated incidents involved substantial human-to-human transmission. Some of these incidents were associated with "super-spreaders": particular individuals who got infected and spread the virus to way more people than the average. See https://wwwnc.cdc.gov/eid/article/26/2/19-0697_article for more.

SARS caused by the original SARS-CoV virus indeed seems to be gone, with no cases reported since 2004. The elimination of SARS from the human population occurred via controlling the human-to-human spread through isolation and contact tracing. See https://apps.who.int/iris/handle/10665/70863 for a report on the epidemic and how cases and spread in different locations were handled.

Viruses don't have any agency: they can't decide to do anything. However, humans can, and our best response to outbreaks of novel diseases is to trace the spread and try to limit transmission as much as possible.


Are the cpli and ctli tests time senstive(i.e. is it needed to test right away in order to get accurate results)?

From doing a bit of research, I quote

  The various analytes have different stability in serum. Serum TLI and
  PLI are stable for up to 2 weeks at room temperature. However, serum
  folate shows limited stability at room temperature. Therefore, serum
  samples for folate analysis should be kept at 4ºC for not longer than
  48 hours, but freezing is preferred. Furthermore, folate is light
  sensitive and samples should be stored in the dark or wrapped in foil (reference).

So, it should be fine if the tests are conducted in two weeks.


Assumptions

You are ignoring recombination and mutations. If you were to add these things, then this probability would be extremely smaller. In apparence, it would be infinitely smaller. It makes no biological sense to make such assumption but for the sake of the argument, let's assume only segregation happen. We will also assume that the parents are completely unrelated to start with (see @BryanKrause 's comment below).

For on given pair of chromosome

First, for a given chromosome number, both parents must each transmit a different chromosome to each offspring. This happens with probability $\frac{1}{2}$ per parent and therefore $\frac{1}{4}$ for both parents. Then, if the brother transmit the maternally derived chromosome, then the sister must transmit the maternally derived chromosome as well (and vice-versa). This occurs with probability $\frac{1}{2}$. So for a given pair of chromosome the probability to clone the parent pair of chromosomes (assuming no recombination and no mutation) is $\frac{1}{4}\frac{1}{2} = \frac{1}{8}$.

For the whole genome

The probability of this to happen for all 23 pairs of chromosome is $\frac{1}{8}^{23} = 1.69 \cdot 10^{-21}$, that is one chance out of a 1.69 thousands billions billions.

As you ask for the odds, note that for such low probability the odds ratio is pretty much equal to the probability.


Can we knock out Caspase-9 *and* avoid breast cancer phenotype in our mouse model?

The short answer is that it is likely a bad experiment; being that it would be expensive and is not likely to provide useful new information.

The long answer (i.e. why) is identifying an interesting target gene (e.g. caspase-9 in breast cancer) is only the first step, and considerable study of what is already known is required before planning an experiment (especially an expensive one that requires numerous mice).

Caspase-9 is a critical effector of apoptosis through the mitochondrial pathway. Many different signals such as DNA damage, Endoplasmic reticulum stress, etc induce cells to die through this pathway. This is important both in normal development and in preventing cancer. Homozygous deletion of caspase-9 is lethal, the mice will not live to adulthood. (http://www.ncbi.nlm.nih.gov/books/NBK6153/) A conditional knock-out of caspase-9 in breast cancer cells would be needed, not a global deletion.

Furthermore, the given the known functions of caspase-9 this experiment is not likely to provide interesting new information. This pathway is well characterized and known to play an important role in cancer (Resisting cell death; a hallmark of cancer: http://www.cell.com/abstract/S0092-8674(11)00127-9 ) Loss of caspase-9 activity makes cells resistant to apoptotic signals through the mitochondrial pathway(they won't die when they receive these "suicide" signals). This allows mutant cells to survive when they should otherwise die. Cancer cells can also become resistant to this pathway through other means (such as the up regulation of anti-apoptotic Bcl-2 family members.

Many scientists are already studying how to restore normal function of this pathways in various cancers; what do you hope to learn by breaking it that isn't already known (I'm not saying that there couldn't be a good reason, but if you don't have one, you shouldn't do it.)


How are two species with similar phenotypes identified as different?

Species are difficult to define. This is because they form over a gradual continuous spectrum via evolution, one species does not suddenly become two, but lineages diverge (perhaps because there is some kind of barrier - like a mountain range - in the way) eventually reaching a point where we class them as separate species. How we define species is debated but the most generally accepted definition is the Biological Species Concept (BSC). Roughly the BSC defines a species as "a group of individuals that do, or could, successfully breed." Other species concepts do exist, some have their merits, but the BSC is most widely accepted and normally taken with a pinch of salt - it's not always possible to perfectly define a species because evolution and speciation are ongoing processes. Therefore, according to the BSC, two groups can be called different species even if the individuals look identical as long as there is true reproductive isolation.

Reproductive isolation can occur because of physical barriers such as rivers, oceans, mountains, environmental change. This is the cause of allopatric speciation. One species could become split when a subpopulation forms on an island (e.g. if humans take them to an island). If enough time passes without migration they will become reproductively incompatible. Another mechanism is sympatric speciation, when two species form without geographic isolation. This could be by the evolution of new behavioural, morphological or physiological forms which create division within the initial meta-population in to distinct sub-populations which over time become more reproductively isolated. Traits related to reproduction are amongst the fastest evolving and can quickly reinforce speciation (e.g. sperm morphology is extremely varied between species, see Sperm Biology: An evolutionary perspective, chapter 3).

The higher up the tree of biological classification you go the easier it becomes to classify things in to distinct groups, e.g. An oak tree is clearly a plant, and a whale is clearly and animal; further towards species definitions a whale is a mammal and a sparrow is a bird and both are animals; and perhaps less clearly, carrion crows and hooded crows are two different bird species in the Corvus genus. (Formerly these two were considered the same species!)

Obviously problems begin to occur when we consider species that reproduce through means other than sexual reproduction - e.g. bacteria which clonally reproduce. Traditionally this has been done by phenotypic information. We are now in the genomics era which opens new possibilities. This article discusses modern techniques by which utilise genetic similarity & difference between cells to define species and they suggest it to be a good method. However, this article seems to suggest that genomic methods need some refining first before we start classifying species with them.

  Currently, it appears more pragmatic and efficient to preserve the current species definition than to replace it, because it is serviceable as a first level of screening and current phylogenetic knowledge is too limited for a universal and sound change in the definition.

As for whether two species have been reclassified in to one I know there are examples but Google is not throwing up anything and there's nothing I can remember off of the top of my head - if I remember correctly the male and female mallard were once considered separate species because they look so different but I can't find anything to back this up. Species formerly described as one have been split in to two as well - gorilla's are one such example.


What kind of snake is this? Seen on Koh Lanta, Thailand

If the resort is near a water body then it is highly likely that it is a keelback snake.
For determining whether it is poisonous or not it is extremely important to look at the scale pattern on its ventral side(belly). Unfortunately that is not visible here.


This is a Creatonotos gangis

This nice arctiine moth was described by Linnaeus in 1763.
The species  lives in South East Asia and parts of Australia.

C. gangis went viral earlier this year because of a post in The independent where they wrote about a facebook video on the species... I don't know if this is the same video that was popular at facebook, but take a look:

https://www.youtube.com/watch?v=hn1ms8qfqzM

Furthermore, I can tell you that those weird tentacles are in fact scent organs which secrete pheromones in order to attract sexual mates. And also, their larvae cause huge problems because they eat pomegranade leaves


That's a red rhinoceros beetle. Although, "red rhinoceros beetle" is not the correct name. I'm simply observing that it is red, and that it is a rhinoceros beetle. So, according to wikipedia: suborder Dynastinae. Do an image search for "red rhinoceros beetle" and you'll stuff that looks quite similar. Searching google for that specific image show's that it is a 3d printed model. The list of bugs in list of 3d printed models includes something called "Rozenkever". Which is remarkably similar to "Red Beetle" in German.

Golofa porteri perhaps


Difference between "controlled release" vs "prolonged release"

The first box contains Tegretol Retard, which is an old name for what is now known as Tegretol Prolonged Release (medicines.org.uk).

The second box contains Tegretol CR, which means controlled-release (PubMed).

Drugs.com says:

  Your medicine is called Tegretol 200mg prolonged-release
  Tablets/Tegretol CR 200mg Tablets or Tegretol 400mg prolonged-release
  Tablets/Tegretol CR 400mg Tablets but will be referred to as Tegretol
  prolonged-release Tablets throughout this leaflet.

Concluding from that, Tegretol CR200 is the same as Tegretol Retard, which is now known as Tegretol Prolonged Release.

Saying that, it is a doctor who prescribes drugs and who can answer such questions.


What does the word "refractory" in "refractory period" refer to?

From encyclopedia Britannica:

  "After repolarization there is a period during which a second action
  potential cannot be initiated, no matter how large a stimulus current
  is applied to the neuron. This is called the absolute refractory
  period, and it is followed by a relative refractory period, during
  which another action potential can be generated, but only by a greater
  stimulus current than that originally needed. This period is followed
  by the return of the neuronal properties to the threshold levels
  originally required for the initiation of action potentials."

Absolute refractory period = initiation impossible absolutely

Relative refractory period = initiation possible but in greater energy relative to the original required.


Why would a human female have a sexual display despite male biased operational sex ratio?

Sexual arms race.

There is a fine and internally consistent theory that this strategy by females evolved to oppose the strategy of infanticide by males.  Males of many species including primates and possibly humans can increase their own genetic fitness by killing infants that are not their own.  This frees up attention and physical resources of the female to instead have the baby of the infanticidal male.  Lions are famous for this.  But this is in opposition to the genetic fitness interest of the female, who just invested a bunch of efforts gestating and rearing an infant who was then killed.

My favorite writer on this is Sarah Hrdy.  From the Wikipedia article on this\

  This is where the idea of sexual counter-strategies comes into play.
  Hrdy theorized that by mating with as many males as possible,
  particularly males who are not part of the colony, mothers are able to
  successfully protect their young, as males were unlikely to kill an
  infant if there was the slightest chance that it might be their own.

This explains why women have the sexual displays referred to in the OP.  Other aspects of female human biology match.  Humans keep big breasts so they always look like they are lactating (compared to other animals) - to keep males guessing.  There is no external sign to indicate when a human is ovulating.  Females of other species are receptive and mate when they are ovulating - humans can mate any time.

A strategy of keep the guys guessing.  If one time he had sex with a given female, probably he shouldn't kill the kid.  Maybe it is his?

An interesting (& extremely arguable!) corollary to this is the premise that human culture in its entirety is the male countermeasure to this prehistoric female defense against infanticide: that male dominated culture is a method to ensure paternity.


Did the construction of the Panama Canal lead to a huge change in the local marine ecology?

The panama canal is not just a long contiguous connection between the two oceans as you might think. It operates under a system of locks of varying height because the surrounding region is actually fairly mountainous, so a ship has to enter a lock, let it fill until equilibration with the next lock whilst the boat rises, the barriers open, the boat moves into the next section and the process repeats. It is fairly unlikely much wildlife would be able to pass through this system thus not causing the vast ecological effects you might imagine. https://www.youtube.com/watch?v=hoQ7RHyG-EA this link visualises it for you :)


Short answer
Sleep negatively impacts attention, which in turn impairs balance control in cognitively challenging situations.

Background
Schlesinger et al. (1998) argue that under normal conditions, postural control appears to be automatic, and to require little or no attention in young, healthy adults during quiet standing with full sensory input. However, postural control appears to require increased attention when sensory integration or motor coordination are required. Examples of such challenging conditions where increased attention is required are situations during reduced or conflicting sensory input conditions, or when one is subjected to balance perturbations. The regulation of attention, in turn, is dependent on sleep, because sleep deprivation causes deficits in attention. Hence, although sleep deprivation per se has little or no effect on standing postural control, it can impair postural balance when one has to perform a cognitive challenging task.

Reference
- Schlesinger et al., NeuroReport (1998); 9(1): 49-52


Should we be looking for extra-terrestrial life on comets?

Yes we should be and we are! Scientists have been analysing cometary material - but its a challenging task. The problem with looking at meteoritic material from comets on Earth is that it is generally contaminated with material from Earth. In addition, meteorites get physically altered during their passage through the Earth's atmosphere due to the high temperatures of re-entry.

So, the trick is to send missions to the comet. However, then the difficulty is in designing a mission that can analyse samples in situ. NASA's Stardust mission got around this by sample return to Earth. The probe visited comet Wild-2 and found the amino acid glycine among other interesting organic compounds. However, no evidence of life was found (metabolic products, organisms etc.) Further missions to comets (and asteroids) are planned, but they are not going to explicitly look for life.

Elsila, J.E., Glavin, D.P., & Dworkin, J.P. 2009, Meteoritics and Planetary Science, 44, 1323


The t locus, which is described in detail in this book by Robert Trivers, is the classic 'outlaw' or 'selfish' gene.

If a heterozygous (single) t allele is present in the paternal mouse, the t locus is evident in sperm 95% of the time.  Talk about "Breakin' the Law"!  As a locus whose main phenotype seems to be for mitotic cheating, t seems to convey little or no benefit to the other genes by way of helping the host survive.  t/t homozygotes are sterile.  Nice summary here.