Question about flux and changes in net flux of molecules across a membrane

Diffusion is just the random movement of particles. Over time, the solute will randomly distribute throughout the entire available volume. Under initial conditions, there is no solute in side 2 and so it cannot move to side 1 (thus flux from side 2 to side 1 is 0). At equilibrium, the net flux is 0 but there is still flux from side 1 to 2 and from side 2 to 1 (which is equal and opposite) due to the random motion of the solute. So, flux from side 2 to 1 goes from 0 at initial conditions to some non-zero value at equilibrium (ie it increases).


How do we know that our genetic similarities to other species is actually due to common ancestry?

We don't know, and we never will. Science doesn't work that way. But evolution is the simplest hypothesis that is both falsifiable and consistent with lots of experimental data. Therefore it is the currently accepted scientific theory.

I would agree that genetic similarities between current species does not in itself suggest that they evolved from a common ancestor. But knowing the genome sequence of various species let's you do much more than simply measure pairwise similarity between species. The structure of genetic variation (losses, duplications, inversions, mutations ... ) also fits with evolutionary models. And crucially, genome sequences confirm predictions made by the evolutionary theory --- evolution is not just a post-hoc explanation of data, it has actually been tested many times over, and has never been falsified.

A good example is the sequencing of the human and chimpanzee genomes. We knew long before any genome was sequenced that humans have 23 chromosomes (23 pairs), while chimpanzees have 24. If the theory of evolution is correct and we do have a common ancestor, then that ancestor should have 24 chromosomes, like the chimps do, and it must be that in humans, one chromosome is a fusion of two ancestral chromosomes$^*$. This is a strong, testable prediction: if we don't find this arrangement of chromosomes, then evolution is proven wrong! In the 1980's, the sought fusion chromosome was found using high-resolution cytogenetic banding: it's chromosome 2. Modern genome sequencing later localized the precise fusion point on the human chromosome.

Also, the fossil record provides a timeline, not just a bunch of more or less similar organisms. In general, we don't find old fossils of modern-day animals (including ourselves), but we do find old fossils of species that no longer exist today. And when piecing together the findings, it looks like there is a sequence of gradual changes over time. That's a pretty good clue. What hypothesis might fit this data?

If you are suspicious about the theory of evolution --- which is fine, you should think critically about everything in science! --- then you must look for an alternative hypothesis which is falsifiable and fits the data. (Note that "god made everything" is not a falsifiable hypothesis, since it makes no testable predictions, and therefore not relevant to science.) If you come up with anything, let us know!

$^*$ As pointed out in comments, a priori one could imagine other rearrangements between the ancestor genome and the chimpanzee/human genomes that give the same result, but I believe this is the simplest hypothesis.


What is the best way to make a phylogeny from a list of genera?

16S phylogeny would only work for bacteria and archaea unless you are talking about mitochondrial or chloroplast 16S rRNA. Your phylogenetic marker choice should depend on which phyla you are looking at. I suggest you try using Ef-tu if your genera are highly diverse
http://www.scs.illinois.edu/schulten/tutorials/ef-tu/eftu_tutorial.pdf

Once you have a tree in Newick format, iTOL has some nice web tools for overlaying data on trees
http://itol.embl.de/itol.cgi


For a recombinant pUC19 plasmid with cut sites at Hind III and EcoO109i, does lactose need to be present for the gene of interest to be expressed?

I would rather use the synthetic analogon IPTG for induction of genes behind a lac promoter, as they are not getting degraded (or at least much slower than lactose) and thus give a much stronger induction signal.

You will need to test the optimal IPTG concentration, but as a starting point I would use and endconcentration of 1mM. If this is not optimal (to much unsoluble protein or not enough), you can change the concentration in either direction. To start, use an overnight culture to inocculate a fresh culture in the morning and follow up the OD600 until it reaches 0.6-0.8 before adding the IPTG.


Why do Arctic predators accumulate vitamin A?

The phytoplankton at the bottom of the food chain have high levels of vitamin A and precursors like beta-carotene.  At each step up the chain, vitamin A bioaccumulates.  Top predators in the Arctic deal with this by storing the vitamin A in the liver (bears, cetaceans) or blubber (pinnipeds).

This is the same mechanism that causes accumulation of pesticides like DDT in animals.  https://en.wikipedia.org/wiki/Bioaccumulation

Carotenoids are part of the photosynthetic system, and also protect the organism from sunlight.  Phytoplankton are unicellular, so each cell needs protection.  Therefore land plants contain much less carotenoids, since most of the cells are interior and protected from the sun.  For example, grains, roots, and wood have very low levels of carotenoids.

This occurs in polar regions due to up-welling nutrient-rich waters supporting high productivity.  Temperate and tropical deep ocean regions are typically deserts due to low nutrient levels, particularly iron and fixed nitrogen.


Below which temperature human muscles don't work?

If you dissect striated muscle out of most-any organism, the actual contractile apparatus works over a wide range of temperatures. So that's at the single-muscle-fiber scale. The muscle itself continues to work at all (thawed) temperatures below body temperature -- the problem comes with its regulation.

The shivering response -- a centrally controlled  involuntary contractile pattern -- overwhelms voluntary muscle control. So the mechanism behind loss of muscle coordination in hypothermia is the same as the shivering mechanism. When the core temperature drops, the midbrain starts over-riding voluntary control of the muscles. When the core temperature drops far enough; around 32C, the shivering often slows down or stops. Voluntary movement becomes compromised probably because the brain simply isn't working; neuron firing rates are so slow that sensation, processing, and motor responses are all critically impaired.

The feeling of numbness does not actually directly accompany a loss of muscle contractility. You can walk pretty much indefinitely on frozen feet if you can keep your balance (and you keep your core temperature up.) Lots of people survive severe frostbite of their feet (their feet do not often survive, however.) The reason why it seems your hands don't work when they get cold is that you can't feel what you're doing (note; your hands can be much colder than your core body temperature.) But the muscles themselves work right up until they freeze solid.

UPDATE:
 Here's a paper that directly addresses the scenario posed by OP -- the decrease in grip strength with temperature.   Figure 1 of that paper illustrates their experimental setup; they measure the contractile strength of the index finger while manipulating the temperature of the rest of the hand. They show that contractile function is impaired with temperature and look at temperatures as low as 12C.

They measure as much as a 50% impairment on twitch tension upon cooling to 12C. It's interesting that they review results suggesting that some of this effect is intrinsic to the muscle fiber (not neurological), showing that I should refine what is meant by "continuing to work" in my opening paragraph. (I meant having an ability to generate contractile force when equilibrated in solution containing sufficient ATP and Ca$^{2+}$, not the ability to contract optimally.) For fun, I linearly extrapolated the final arm of Figure 5 and found that the 'voluntary tension' approached 25% at 5C. This suggests that total failure of the voluntary contraction happens somewhere below the freezing point of water (muscle would freeze at a temperature lower than 0C because of colligative effects.)


Tiny dark-colored bug ID in Amman-Jordan

These are very likely flour beetles (Tribolium spp) of some kind. These small (~3mm) reddish-brown beetles are some of the most widespread and common pests of stored food products worldwide [source].

 Left: red flour beetle; Right: confused flour beetle. Photo credits: Rebecca Baldwin (left); James Castner (right)
The photo is too blurry to be able to differentiate between the most likely candidates: red flour beetle (T. castaneum) and confused flour beetle (T. confusum).

You can learn more about differentiating these insects here and here, and you can find more general information about them via UF/IFAS.

Distribution: Both species are essentially found worldwide; This UF/IFAS page provides a bit more nuanced explanation of their distribution:

The red flour beetle is of Indo-Australian origin (Smith and Whitman) and is found in temperate areas, but will survive the winter in protected places, especially where there is central heat (Tripathi et al. 2001). In the United States, it is found primarily in the southern states. The confused flour beetle, originally of African origin, has a different distribution in that it occurs worldwide in cooler climates. In the United States it is more abundant in the northern states (Smith and Whitman).

Extermination tips are available via epetsupply.com:

Prevention is key!
Keeps your home clean and free of food/crumbs
Sticky traps and pheromone traps

If I had to guess, I'd guess from your poor images that you have red flour beetles, but honestly it doesn't much matter from a pest-control standpoint.

The red and confused flour beetles live in the same environment and compete for resources (Ryan et al. 1970, Willis and Roth 1950). The red flour beetle may fly, especially before a storm, but the confused flour beetle does not fly. [source: UF/IFAS]

UPDATE:
Alternatively, now that I've looked at your picture with such a small specimen, it could be possible this is another "grain beetle": Ahasverus advena, the foreign grain beetle. From Wikipedia:

 Source: Wikipedia

Description:
The foreign grain beetle is approximately 2 mm (1⁄12 in) in length. It can be distinguished chiefly by slight projections or knobs on each front corner of the pronotum, and its club-shaped antennae. The larvae are worm-like, cream-colored and often reach a length of 3 mm before pupating into darker adults. Males and females are identical in appearance both as larvae and adults. The adult is usually reddish brown, or sometimes black.

Distribution
The foreign grain beetle is found in tropical and temperate regions [and is distributed all throughout the world -- see Spanish translation of Wikipedia page].


What is the relationship between W, X, Y and P, M retinal ganglion cells?

Short answer
X = P = midget = β
Y = M = parasol = α
W = γ

Background
First off, P and M cells are not equal to parasol and midget cells; on the contrary - P cells are midgets and M cells are considered to be parasols.

X, Y and W cells are used to denote different retinal ganglion cells in cats, as proposed by experiments Enroth-Gubel & Robson (1966). As you already indicate, these cells have different physiological response properties. X and Y cells have the standard center-surround distribution of their receptive field, X cells having linear additive response properties in center and surround and Y cells nonlinear properties. X cells therefore have predictive responses such that responses can be predicted to be maximal (e.g. light shining on the ON center and no light stimulation on the OFF surround). Y cells tend to respond in more complex ways. W cells do not have a center-surround structure (Bruce et al, 1996).

Based on morphology, retinal ganglion cells in the cat have been labelled α, β and γ cells, which are thought to correspond to the physiological classes of Y, X and W cells, respectively (Boycott & H. Wässle, 1974).

The P and M division was introduced by De Monasterio & Gouras (1975) based on monkey experiments. P and M refer to the parvocellular and magnocellular connections retinal ganglion cells in monkeys make in the LGN of the brain. Both types of cells have a center-surround receptive field structure like X and Y cells in the  cat. P cells show color opponency and respond to specific wavelengths of light, and are involved in color vision. P cells respond to a range of wavelengths and respond most vigorous when different light intensities illuminate the center and surround (Bruce et al, 1996).

P cells are considered to be mostly midget ganglion cells, and equivalent to β cells of cat. M cells, on the other hand are considered to be mostly parasol cells and resembling α cells (Kolb, 2001).

References
- Boycott & H. Wässle, J Physiol (1974); 240(2): 397–419
- Bruce et al, Visual Perception (1996); 3rd ed. Psychology Press
- De Monasterio & Gouras, J Physiol (1975); 251(1): 167–95
- Enroth-Gubel & Robson, J Physiol (1966); 187(3): 517–52
- Kolb H. Webvision (2001). Salt Lake City (UT): University of Utah Health Sciences Center


Actually we aren't that good at localizing cancer cells.
There need to be around 100,000 cancer cells at a single location for the cancer to be visible on fMRI.

If you want to treat a cancer via chemotherapy it's good to be able to see the cancer. It allows you to see whether the drug you are giving works.

When dealing with a metastasized cancer where you don't think you know every location in which cancer is hiding it therefore often makes sense to avoid to take out everything you can see via surgery.


EDIT -- I think this is actually a black stem aphid (Cinara confinis) [see below]

I think these are Hemiptera, and I doubt they are pests. They probably came from the christmas tree (which usually brings hundreds of arthropods into your house). It is a bit hard to see from your pictures (blurry, no clear underside), but my initial guess would be a nymph from Hemiptera (True bug), for instance from the Coreidae family (look at a google picture search at nymphs for some examples). An alternative could be nymphs from Psocoptera), which can look a bit similar. A clear difference between them is in the mouthparts, where Hemiptera have a rostrum (a "straw", sucking mouthparts), which should be seen from the ventral side, while Psocoptera has biting mouthparts. Your second ventral picture seems to show a long rostrum along the underside, which would point directly at Hemiptera. I don't know of any indoor Hemiptera pests (except ones that might attack house plants), but I might be mistaken.

This is just shown as an example, and is not likely to be the correct species, but here are the nymph stages of the common Coreus marginatus, just for comparison:

(from http://www.ukwildlife.net/heteroptera/coreidae/coreus_marginatus.html)

Here is a picture clearly showing the rostrum (see arrow):

(from http://www.fao.org)

Another possibility could be that they are aphids. This is still within Hemiptera (but not Heteroptera), and they also have a rostrum. Aphids have a pair of "tubes" (cornicles) coming out of their backs where they can extrude defensive compounds, and your first picture shows something that might be cornicles (the pointy things towards the back). However, to me, they seem to lie towards the side and look like the type of spikes or thorny sides that many Heteroptera have (a suborder of Hemiptera). Your individual also seems to have flattened edges of the hind body, which e.g. many Coreidae have. Again, clearer pictures would separate these possibilities. It would also be useful to see the number of antennal segments clearly.

EDIT
That said, I looked at some pictures of aphids living on coniferous trees and they can be fairly similar to your specimen. I actually think Cinara confinis is very likely (or another species in the same genus). This species is circumpolar, found in France, and often lives on Abies:

(source: free.fr)

(Cinara confinis, both pictures from http://aesgsf.free.fr/V5/hemipteres-divers-de-picardie-hemiptera-cinara-confinis.html)


Could we use this technology to completely eradicate from the world
  all species of mosquito that prey on humans?

Yes, implemented correctly, a gene drive has this capability.

  Also, could we accurately predict the extent of the resulting
  ecological disruption so we could decide if it was worth it?

The current scientific and political consensus is that, no, we can't predict the potential consequences with high enough confidence to move forward with such a large-scale manuever.

One of the leading scientists studying and improving gene drives, Kevin Esvelt at the MIT Media Lab, instead supports a "daisy chain gene drive" which is pre-programmed to weaken with each successive generation, allowing humans to effectively control the spread of gene drives to a specific geographic area and time frame.


Garden Hose Analogy for Blood Vessel Resistance

It comes down to the distinction between velocity and flow rate.
While you are right that the water would leave a an increased velocity if you put your thumb over the end of the hose, this is deceptive, because the water is exiting the closed system, so it can go absolutely anywhere.  So the fact that the velocity is increased could give one the impression that the flow rate is increased, but in fact it is the inverse.
Imagine that instead of putting your thumb on the end of the hose, you pinched the hose in the middle instead. This would result in the water flowing out of the end of the hose at a reduced flow rate (lower volume of water coming out per minute) and velocity (lower speed of the individual water particles).  Why?
It might help to take a snapshot of the place where you are pinching the hose.  the pressure behind the pinch zone goes up, causing the water to pass through the pinch zone at a faster velocity. However, because the hole is smaller, less water is able to pass through.  When it reaches the other side of the pinch zone, it slows down again because it has a very low pressure, and the smaller volume of water must fill the entire tube. However, because the flow rate was lowered because of the pinch zone, the amount of water at the end of the pinch zone is lower.  Consequently, the water flows slower and the flow rate is reduced simultaneously.
Another analogy that might help would be the comparison between a garden hose and a fire hose.  Let's say they have the same flow rate (same volume coming out of the hose per unit time).  You can immediately realise that for the garden hose to put out the same amount of water that the fire hose is putting out in a minute, the water would have to be flowing many times faster in terms of velocity.

Furthur reading

Grunwald JE, Petrig BL Riva CE, Sinclair SH. Blood velocity and volumetric flow rate in human retinal vessels. Invest. Ophthalmol. Vis. Sci. 1985;26(8):1124-1132. Available online: https://iovs.arvojournals.org/article.aspx?articleid=2159754
Baker M, Wayland H. On-line volume flow rate and velocity profile measurement for blood in microvessels. Microvasc. Res. 1974;7(1):131-143. Available online: https://doi.org/10.1016/0026-2862(74)90043-0


Estimating RPM to RCF in Methods from Older Papers

I am not sure about what they used in 1958 (perhaps Sorvall). However you may look at recent papers for ECM protein isolation (if that was your objective).
Have a look at this article.
From materials and methods:

ECM protein isolation.
Fibroblasts or A431 cells were removed from the
surface of the culture plate with 2 mM EDTA in PBS for 3–5 min at
37⁰C. Detached cells were discarded, and remaining ECM proteins
attached to the surface of culture plates were washed with the same
solution. Cell removal was controlled under the microscope. After
cells were completely removed, matrix proteins were covered with 5%
acetic acid and incubated at 4⁰C overnight. Then, acetic acid was
removed and exchanged with a buffer containing 125 mM Tris-HCl, pH
6.8, 0.1% SDS, 10% glycerol, 1% DDT, 0.05 mM PMSF, protease inhibitor cocktail (Roche, Germany), and incubated at 37⁰C for 1 h. Proteins
were removed with a scraper. The procedure was repeated three times.
All protein extracts, including acetic acid, were combined and ECM
proteins were precipitated by five volumes of acetone. After
incubation at –20⁰C overnight and centrifugation at 7000 g for 15 min,
the protein pellets were dissolved in an appropriate buffer for
further analysis by one- or two-dimensional gel electrophoresis.
In addition, we obtained a Triton X-100-soluble fraction of ECM
proteins. Cells were removed as described above; dishes were filled
with 1% Triton X-100 and incubated at 37⁰C for 30 min. The extraction
was repeated three times. The following procedure of ECM extraction
was the same as described above. Samples obtained from both fractions
were dissolved in a buffer for one-dimensional (Laemmli) or
two-dimensional (rehydration buffer containing 8 M urea, 2% CHAPS, 20
mM DDT, 0.1% Triton X-100) electrophoresis. Proteins that remained
after Triton X-100 extraction were dissolved in Laemmli sample buffer.


Finding a easy and cheap method for dyeing dNTP

There may be such a dye, but I'm not aware of it.  The standard way to measure dNTPs, and nucleic acids in general is by absorbance at 260 nm. This article has a table of molar extinction coefficients for dNTPs (Table 10.2). They are

        wavelength      molar extinction coefficient
dATP    259 nm          15,200
dCTP    280 nm          13,100
dGTP    253 nm          13,700
dTTP    267 nm           9,600

In practice for routine work with DNA you can use 260 nm and assume that an absorbance of 1 corresponds to [DNA] = 50 µg ml-1. Using an average of the values in the Table, and disregarding the fact that these are actually at different wavelengths, and using an approximate average dNTP MW of 500, I calculate an absorbance for a 50 µg ml-1 solution of all 4 dNTPs as 1.3, so that's a reasonable agreement given all of the assumptions I've made.

There are fluorescent dyes that can be used to measure DNA, but these rely upon the presence of stacked bases, so are not useful for free dNTPs.

So, bad news if you don't have a UV spectrophotometer. There are plans available for construction of simple spectrophotometers using Lego and a few optoelectronic components. These tend to use LEDs as a light source, but I don't know if UV LEDs are available.


What are the factors that contribute to genetically identical individuals behaving differently?

Your question has actually more to do with developmental biology and the origin of phenotypic variance in populations than with neuroscience.
Here is a list of factors which variance explain observed phenotypic variance in a population:

Genetics (incl. additive, dominance and epistatic variances)
Environment (incl. macro and micro environments)
Developmental noise (incl. cellular noise)
Epigenetic
All the covariances among above factors

Of course, when you consider a pair of monozygotic twin as your population, there is little to no genetic variance. They will also likely experience little epigenetic variance. Assuming they live together, practice the same sport, eat the same type of food, etc... then they will also experience little macro-environmental variance. Micro-envrionmental variance and developmental noise are probably the main factors causing these two hypothetical twins to differ.
You might want to read the post Why is a heritability coefficient not an index of how “genetic” something is? to better understand the current post.


What is the difference between a "semi-contracted" muscle and a "contracted" muscle?

If you consider the length of a muscle can vary from resting length to shortest length, my guess is that semi-contracted is somewhere in between. I believe that spine-health.com isn't being entirely clear with their definitions.


Are these 3.5B year old fossils the oldest on earth?

Yes, the study was peer reviewed and published less than a month ago (Dec 18, 2017) in PNAS, among the most prestigious journals in science by qualified experts. They could be wrong of course, like all science. But there is no reason I can see to doubt their work.


Introducing evolution into the Hodgkin-Huxley equation

Although you mention evolution, I think what your question is really asking is in your last paragraph: what happens to conduction within dendrites and axons when geometry changes. There might be some evolutionary implications of this question, but you will also find vast variations in geometry among neurons in any one organism, as well.

You might want to look into expansions of Hodgkin-Huxley into compartment models that allow you to test the influences of geometry, see wikipedia for a list of different models at different scales of complexity.

There is a tool available called NEURON that is good for student or curious non-student experimentation, though you will have to read the documentation and hopefully find some examples that are close to what you want and then tweak them.


Why is sugar absorbed very fast into the blood stream?

In short, sugars are absorbed quicker than proteins and fats because they pass through the stomach quicker and their digestion is simpler.

Sugar can be absorbed through the mouth mucosa when applied as a sublingual gel, as discussed here on Biology SE: Is sugar absorbed into the bloodstream through the walls of the mouth?, but probably in much smaller amounts during usual eating/drinking followed by swallowing.

SUGARS

Not all sugars are absorbed at the same rate.

Glucose and galactose do not need to be digested and can be quickly absorbed in the small intestine via sodium–glucose linked transporters (SGLTs) - sodium acts as a cofactor that stimulates glucose and galactose absorption (Lumen Learning).

Fructose also does not need to be digested but is absorbed much slower than glucose via GLUT5 transporters without the help of sodium (Lumen Learning).

Sucrose needs to be digested in the small intestine with the help of the enzyme sucrase to glucose and fructose, which are then absorbed. Glucose stimulates the absorption of fructose (Food and Agriculture Organization). This means that glucose and fructose from sucrose will be absorbed slower than glucose alone, but faster than just fructose alone.

Lactose needs to be digested to glucose and galactose, which prolongs the time in which they can be absorbed.

The absorption rate of various sugars is reflected in their glycemic index (the rise of blood glucose levels after ingestion): GI for glucose = 100, sucrose = 65, lactose = 46, fructose = 19.

STARCH

Starch is not digested in the stomach, so it can pass through it quickly, and is then, in the small intestine, quickly digested to glucose with the help of the enzyme amylase. The glucose from plain starch is absorbed almost as quickly as when ingested as glucose alone and faster than fructose, sucrose or lactose. This is evident from high glycemic index of foods made mainly of plain starch: cornflakes (81), instant oats (79), potatoes (78), rice porridge (78), white wheat bread (75).

FIBER

Foods high in dietary fiber slow down gastric emptying and thus absorption of nutrients (Faseb).

PROTEINS

Proteins need to be digested in the stomach by the enzyme pepsin (which slows down gastric emptying) and then further in the small intestine by peptidases into amino acids, which can be absorbed. Slow gastric emptying is the main reason for slow absorption of proteins (Diabetes Care, Experimental Physiology).

FATS

Fats are not digested in the stomach but they slow down gastric emptying, so they are absorbed slower than carbohydrates (JCEM, Vivo Colostate).

LIQUID vs SOLID MEALS

Liquid meals pass through the stomach quicker than the solid ones, so glucose from sweetened beverages will be absorbed quicker than from whole fruits (Vivo Colostate, JCEM).


Bimodal frequency distribution of size of protein loops

A curve of this type, showing a bi- or multi-modal distribution,
  suggests two or more constituent species
  in the population. In this case this is borne out by further analysis
  in the paper of different types of secondary structure components
  anchoring the loop, the peak at low numbers of amino acids reflecting
  the loops connecting β-strands in anti-parallel β-sheets.

The second frame (B) of Figure 2 is shown below (dashed line):

Anti-parallel β-sheets are abundant in proteins, and in many — although not all — cases adjacent strands are connected by short (four- or five-amino acid) loops such as the β-turn, the β-hairpin or the β-bulge loop.

Repeating small loops are especially well illustrated in β-sheets displaying β-meander:

The β-meander motif from the outer surface Protein A

Examples in larger domains of the β-barrel and immunoglobulin type also show some larger loops.

Beta barrel of green fluorescent protein, showing loops at end of strands

Immunoglobulin domain of PDB 5IML showing β-sheet with loops connecting strands


Are RNA cleavage sites always polyadenylated?

This answer attempts to cover only the question of mRNA processing. It does not address the polyadenylation of non-coding RNAs.

As far as I can see from the recent review by Neve et al. (2017) cleavage and polyadenylation are tightly coupled. It is interesting, in this regard, that histones mRNAs which lack polyA tails, have a different structure, lacking the canonical AAUAAA, at their 3ʹ ends (see review by Marzluff et al.).

As distinct enzyme activities are involved in cleavage and polyadenylation, it would, I imagine, be possible (either genetically or chemically) to disrupt the protein complex responsible for polyadenylation and hence prevent it occurring (this has probably been done). However this would not be physiologically relevant.

There is an earlier review by Tian and Graber (2007) of the sequence requirements of the cleavage site which makes no distinction between cleavage and polyadenylation.

However this is not my field, so others may have additional information I have missed.


Why aren't nucleic acids on Nutrition labels?

This FAO report can tell you all about food analysis and why things are and aren't on the label: http://www.fao.org/docrep/006/y5022e/y5022e03.htm#TopOfPage

  First, not all nitrogen in foods is found in proteins: it is also contained in variable quantities of other compounds, such as free amino acids, nucleotides, creatine and choline, where it is referred to as non-protein nitrogen (NPN). Only a small part of NPN is available for the synthesis of (non-essential) amino acids.

The DNA in food would contribute to the nitrogen content. Then (using a food-specific "Jones" factor) total nitrogen content is converted to protein content. So in a way it's already there.

Listing DNA separately would require extra testing, and also the difference in daily use would be negligible. There's not that much DNA in food anyway and, like protein, DNA can be converted into new protein and energy. The Jones factor already accounts for this.


Has a primate species ever weighed the average mass of a tonne (1000 kg)?

There is no specific reason why a primate couldn't weight a metric tonne. You can look at mammals evolution and notice that the primates belong to the clade Euarchontoglires which also contains rodents, treeshrews or rabbits. So basically these species most likely had a common ancestor that was very small.

Primates are currently the biggest animals of that clade. Great apes are the biggest primates. Gorillas at about 150kg on average are the biggest (by weight) currently non-extinct great apes. Chimpanzees, Orangutans and Humans are approximately equals at 75kg. The biggest known primate, now extinct, is the Gigantopithecus which was probably a sort of giant Gorilla twice the size of what you know as Gorillas (200-300kg), so still well short of a tonne. The biggest non-extinct rodent is the Capybara (you can see one at the Cosmocaixa in Barcelona). But the biggest known extinct rodent was the Josephoartigasia and did weight 1000kg.

Euarchontoglires sister clade is Laurasiatheria which does contain many animals bigger than 1000kg, such as Bisons, Rhinos, Girafes, Orcas, Walruses... These 2 clades belong the Boreoeuthenia clade, whose sister clade Atlantogenata also contains many animals heavier than 1000kg (most notably elephants). So evolutionarily primates would have had plenty of time to become as big as rhinos, but it looks like this group found its ecological niche in staying relatively small (although humans and chimps are not that small as compared to rodents or rabbits). Getting big is not always smart as we know from mammals surviving the Cretaceous extinction thanks to their tiny size.

Evans et al. (2012) tried to estimate the maximum rate of evolutionary body mass increase in mammals (through natural selection, it is likely you could force this process to be much much faster). They found that it took about 1.6 millions generations for body mass to increase a 100-fold in terrestrial mammals. So a back-of-the-envelope calculation tells you it would take about 30 million years for current primates to reach 1000kg. They also point out that the aquatic cetaceans grew much faster than any terrestrial mammal, suggesting that being terrestrial strongly limits growth rate. They also point out that macroevolutionary growth rates are far slower than what would be predicted from microevolutionary rates, for reasons still unknown.

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

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

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

Evans, A. R., Jones, D., Boyer, A. G., Brown, J. H., Costa, D. P., Ernest, S. M., ... & Harding, L. E. (2012). The maximum rate of mammal evolution. Proceedings of the National Academy of Sciences, 109(11), 4187-4190. https://www.pnas.org/content/pnas/109/11/4187.full.pdf


How is Microenvironment strictly defined?

The meaning of the term microenvironment depends on the scale of the system that you're looking at. It's a sort of weasel word that loosely means "context" or "stuff in the immediate surroundings of the system of interest that has some kind of an effect on it". I've seen it used to describe everything from the chemical microenvironment of a cell (e.g. a hormone gradient) to the electrostatic microenvironment of a single amino acid residue in a protein (e.g. the field from nearby charged residues).

Conceptually it's similar to the "surroundings" in the "system and surroundings" framework from statistical physics.


You are not telling, what you do, but I think itis western blot - and for this application it is not important to know which isotype your antibody has. The secondary antibody (which is supposed to bind the primary) has to be directed against the isotype (IgG for example) and the species in which the primary antibody was made, in your case this would be this would be anti-mouse or anti-rat IgG. Since most commercially antibodies in the lab are IgG people usually don't think about it.

The reason is that the secondary antibody is directed against the Fc part of the primary antibody (which has a species specific sequence) and even with the differences in the sub-classes due to different assembly of the light and heavy chains this will not be detected by the secondaries. See the figure (from here) about the schematic differences:

With a careful selection of the peptides used for immunisation it is possible to generate secondary antibodies which can be used to distinguish between sub-classes.


Effect of recombination on the rate of loss of genetic variation

I found a key paper for myself from an issue of Nature Reviews Genetics last year. It discusses and reviews how recombination affects the rate of genetic variation at the sequence level.

A key concept is that of selective interference, which is what I had stumbled across in the question, this is when the efficacy of selection is reduced because "recombination fails to break down linkage disequilibrium at selected loci." Simply, a beneficial mutation in a system of no recombination is only as fit as the background it is in, if recombination is extremely high (no LD whatsover) then the fitness is defined only by it's own effects. This means that recombination can reduce polymorphism because selective interference will reduce the speed at which non-neutral alleles are fixed or lost.

However, recombination maintains polymorphism, because without it there is a greater potential for hard sweeps, soft sweeps, partial sweeps, and background selection to all remove genetic variance. For sweeps a beneficial mutation will drag any mutations it is linked with to fixation, the further from the allele the weaker that effect is.

It seems that over riding effect of recombination is to maintain genetic variance despite the increased rate at which an mutation can fix when there is no selective interference because it reduces the polymorphism reducing effects of sweeps and background selection.

  "It is expected that neutral genetic variation will be systematically
  depleted in genomic regions with little recombination."


How does a TOPflash/FOPflash assay work to detect beta-catenin protein expression?

From what I can understand, TOPflash is a luciferase reporter plasmid that contains two sets of 3 copies of the wild-type TCF binding regions. If the canonical Wnt signaling is activated, beta-catenin will translocate to the nucleus to associate with TCF/LEF transcription factors to activate transcription of Wnt target genes. Since this is a luciferase plasmid, you should see an increase in relative luciferase activity when substrate is added. If Wnt signaling is inhibited, you will see loss of luciferase expression. The FOPflash is used as a negative control because the TCF binding regions upstream of the luciferase gene is mutated so even if beta-catenin translocates to the nucleus to activate TCF-mediated transcription, you should not see any luciferase activity.

Hope this helps.


Name/term for mechanisms by wich the relative size/number of cells of some tissue/organ are preserved

'Eutely' is the term used for organisms with a fixed number of somatic cells. I'm not aware of any term for sub-organismic structures.


Splice junctions are the exon-intron junctions, at which splicing takes place.
Splice junction pairs are the pairs of such junction (to cut an intron you need to splice in two junctions).
So, you are almost there, since two exons will be joined in correspondence of two subsequent splice junctions.
You might find these slides useful (slide B-6)

EDIT:

As Adam pointed out the slides are no longer available. I have no idea on where they are gone, but I suggest referring to the following wikipedia pages for an introduction:

RNA splicing

Exon junctions

Alternative Splicing


Almost certainly a spider belonging to the genus Scytodes. It largely resembles the species S. thoracica with very similar markings to the picture above. It is a common spider in the United States, and is often found in houses.


Your picture most likely shows Lichnanthe rathvoni of the family Glaphyridae.

The older answer is almost certainly not correct in any of its guesses; all of the possibilities listed are Palaearctic (see the sites https://fr.wikipedia.org/wiki/Epicometis_hirta, https://en.wikipedia.org/wiki/Tropinota_squalida, and http://www.coleo-net.de/coleo/texte/oxythyrea.htm for confirmation; the first and third will need translating for those not fluent in French and German, respectively).

Referring to Part V of M. H. Hatch, The Beetles of the Pacific Northwest (1971) (which covers the states of Idaho, Oregon, and Washington, and the province of British Columbia, in their entirety, and the western part of the state of Montana), and assuming the subfamily Cetoniinae is correct, I had thought this was Trichiotinus assimilis Kirby; there are inconsistencies between this photo and those provided by bugguide.net (see http://bugguide.net/node/view/22486); specifically, the elytra here are well-separated apically, and the coloration is quite different.  A review of Volume 2 of American Beetles showed me my error: the insect is a member of the family Glaphyridae (formerly a subfamily of Scarabaeidae), and the genus Lichnanthe; returning to Hatch, 1971 shows only L. rathvoni LeConte from the covered area; photos of that species in bugguide.net (see  http://bugguide.net/node/view/115846) show some variation in markings from the photo here (which is to be expected), but are structurally fairly close.

The genus Lichnanthe was most recently revised in the following paper:

Carlson, David C..  1980.  Taxonomic revision of Lichnanthe Burmeister (Coleoptera: Scarabaeidae).  Coleopterists Bulletin, 34(2):177-208.

which is available through JSTOR (a subscription, one-time payment, or access through a university will be needed).


Which is the correct statement on proteins?

Do you have a textbook?  That will definitely have the answer early on in the chapter.  Also, have you tried reading the protein Wikipedia article, in particular the structure subsection.  You will find the information you want there.


Will fruit/seed of a bonsai yield another bonsai plant/tree?

No, seed from a bonsai tree will not automatically produce another bonsai tree. Bonsai are dwarfed due to restriction of root growth in their small containers - unless the offspring are also grown in environmentally dwarfing conditions, they will tend to grow normally.


Synthesis of immunoglobulin Fab fragments: Where can I learn about Fab?

For the generation of Fab-fragments antibodies, (possibly genetically modified) which can be made in large quantities by cells or animals, are used. Antibodies as a whole are not synthesized.

The Fab fragment is obtained from antibodies using the enzyme papain, which cleaves the antibody over the disulfide bonds in the hinge region. This results in two Fab fragments (which contain the antigen binding sites) and one Fc fragment (which contains the constant region of the antibody). See the image (from here):

If you want to go further into the topic, read one of the references below.

Preparation and separation of Fab and Fc fragments from human
immunoglobulin G with papain digestion
Fragmentation of IgG Using Papain


How much variation in the human genome for humans

You are correct in saying that the human genome sequenced in the project was contributed by a dozen anonymous volunteers. However, the final sequence that is used as a standard reference is a somewhat arbitrary construct that represents a collection of consecutive segments taken from one or other of the contributors. It is a haploid sequence, plus a Y and an X chromosome.

Now you ask how different are the genomes of any two subjects, taken at random from a population. Imagine for simplicity looking at your own genome. For each of the 22 autosomes, you know you have two copies, one transmitted from your father, the other from your mother (for the X chromosome you have two copies, if you are a girl). Now imagine comparing the sequence of each of your pair of homologous chromosomes side by side; remember that they are derived from very different individuals (unless your parents are close relatives), so that they will not be identical, as they represent independent evolutionary histories.

Then, the question becomes: how much variation is there between the sequences of your paired chromosomes? And the answer is known: approximately every 1,000 base pairs your chromosomes show a base pair in one chromosome and a different base pair in the other; otherwise they are identical. The sites where this variation occurs are called SNP, for Single Nucleotide Polymorphisms (many other kinds of variation exist, but SNPs are the more common). We can generalize this observation, as it remains true for any pair of chromosomes chosen at random from any pair of subjects. Therefore, we can say that humans are identical for 99.9% of their genomes, whereas the genetic variation responsible for the differences that allows us to recognize ourselves as unique are limited to 0.1% of our genome.


There are lots of biological clocks, or clocks made of biological components. The circadian clock is an important, though complicated, example. There are excellent engineered clocks that form some of the neatest examples of systems / synthetic biology. See for example Elowitz & Leibler's "repressilator" (link, link). The basic idea in all of these is to have gene regulatory circuits with feedback that lead to oscillation of the gene expression dynamics. Books on systems biology, or Philip Nelson's Physical Models of Living Systems (aimed at physicists), are good places to read more.


Why did scientists think humans had 100,000 genes (before the Human Genome Project)?

Human genome is 3.2Gbp (giga=billions of basepairs). If you assume there are 100k genes, this yields around 32kbp (kilo=thousands base pairs) per gene.

Before human genome project, let's say before 1990, people were isolating a lot of genes from human-derived tissues. You can use google scholar to find relevant papers. From quick search, you can see that range is pretty large:

"186,000 base-pair (bp) human factor VIII gene"
"human TF gene spans 12.4 kbp"

So you can see how one might guess "average" size of the gene to be somewhere around 30kbp, if you haven't yet found too many genes. Whereas after genome sequencing, we know that genes are 100-10000 bp long. I think the issue was that there was no enough statistics yet to judge appropriately "average gene size". And as it turns out, the distribution is very funky. You need to isolate a lot of genes to reconstruct that distribution.

By the 1990 phenomenon of the alternative splicing was already known. What perhaps wasn't quite obvious, is how many genes there are, what their real sizes, and how many genes are overlapping


I found this bug in my closet. Could someone help me identify?

The image you provided isn't the best of quality, but I really think it looks like a spider beetle. Anyone else agree?


What vegetation would thrive in the Martian atmosphere?

I'll stick to considering the atmospheric composition, as referred to in the original question: Although there may be some rare exceptions that I can't recall, under normal circumstances all green plants use aerobic respiration with O2 as final electron acceptor for energy production. This means that they require oxygen, which is essentially absent from the Martian atmosphere (0.13%). Even though our hypothetical Martian crop could produce oxygen as a byproduct of photosynthesis, that oxygen would be lost into the atmosphere, and would not be available for respiration.

I believe that under waterlogged conditions some plants can switch temporarily to some sort of anaerobic metabolism as a stress response, but I don't know if this is just to survive or whether the plants can grow in this way - I suspect it is the former.


Since I asked this question I found out what I was doing wrong in searching for Ki (i.e. I thought the Ki ID was the test ligand and hence I was searching for drugs the wrong way) values but also how, I think Goodman and Gilman got its Ki values.

I think what they did was they searched for the hot ligand that gave the most consistent and numerous Ki values and took the average of the consistent Ki values (with an relative tolerance of ~100% between results). Additionally since I knew the data, as is stated in the page displayed above, was taken 30 June 2009 I was able to eliminate some sources that were probably not available on PDSP at the time. Using this I was able to get consistent averaged Ki values in the vast majority of cases (with like, at most a small handful of exceptions).


Molecular animations of, say, protein synthesis, are simplified, but how exactly?

tldr:

Making these things accurate representations is really hard
Accurate representations can be hard to look at anyway, so aren't always good to convey understanding

Molecular dynamics simulations that span long periods can be really expensive because of how computationally demanding they are, and they rely on accurate structural information about all of the molecules involved which isn't always available. The animation you linked might not be an actual simulation for that reason, but you'd have to check for yourself. Really fine grained accuracy probably isn't a priority for making a cool teaching tool like this one, you just want people to understand the just of it and the Brownian motion there might be a stylistic choice. Again, you'd have to chase it up for this specific example, I just want to give you something generalizable to other animations.

To make macromolecules like this actually interpretable by humans it's important to simplify them. One of these simplifications is normally called a 'cartoon', I don't think they guy in your comments was taking a dig at credibility of the video. It's also important to hide all the water molecules because they get in the way of you and seeing what's going on, so that's another way in which it's been simplified.

If you haven't already, have a look at some proteins in the PDB on the structure viewers and switch the mode from the cartoon/ribbons to other models like ball and stick. Ribbons are a useful way to simplify the structure representation so that you can see what the backbone is doing.

Here's one that I like:
https://www.rcsb.org/3d-view/4KEY/1

And you're right, at the systems level of something like protein synthesis, lots of stuff is involved and it's not practical to show all of it. For something like that it's easier to show these processes a a graph (term for connected nodes), check out the KEGG database for examples:

https://www.genome.jp/kegg/pathway.html#cellular

Hope this helps


Why people don't harvest Locusts when infestation happeds?

Locusts have been harvested in Thailand and Australia they call them sky-prawns. They deep-fry them and consume them happily.

http://www.bugsfeed.com/locust

http://www.fao.org/docrep/017/i3246e/i3246e.pdf

In Thailand Orthoptera or
grasshoppers include Patanga succincta,
Locusta migratoria, Acrida sp.,
Cyrtacanthacris tatarica and Oxya
japonica japonica (Thunb.)
(Hanboonsong et al. 2001; RaƩ anapan
2000). All of them are pests of
economic crops such as maize and
rice. Grasshopper species, parƟ cularly
Patanga succincta and Locusta
migratoria, used to be one of the
major pests of maize and rice. Today
they have become one of the most
popular edible insects since they were
introduced for human consumpƟ on
by entomologists − a campaign to eat
grasshoppers had been launched
because control efforts had been
unsuccessful. For example, in 1983
this was launched by local offi cials and
villagers in Prachin Buri Province
collected more than 10 tonnes for use
as food (Lewvanich et al. 1999).*


Are there any methods to quantify H2O2 (hydrogen peroxide) which don't rely on horseradish peroxidase?

Amperometric detection of H2O2 can be performed without HRP, and gives high-resolution real-time readings.

You will find many different type of electrodes that are used in the literature to detect H2O2, including for instance MnO2-coated carbon paste microelectrodes or gold electrodes derivatized with cytochrome c.

Commercial electrodes also exists. For instance these from WPI are based on derivatized carbon fibers (although they do not specify with what, so I would not exclude HRP...)

Another option is that of using the H2O2-sensitive dye H2DCF (dihydro-dichlorofluorescein).


What is the relationship between sexual and natural selection?

You're not wrong, per se, but in practice they refer to two different concepts.  I honestly think the Wikipedia article does a good job, in particular this sentence:

  In summary, while natural selection results from the struggle to survive, sexual selection emerges from the struggle to reproduce.

It also cites Darwin:

  The sexual struggle is of two kinds; in the one it is between individuals of the same sex, generally the males, in order to drive away or kill their rivals, the females remaining passive; whilst in the other, the struggle is likewise between the individuals of the same sex, in order to excite or charm those of the opposite sex, generally the females, which no longer remain passive, but select the more agreeable partners.

The whole argument is moot when dealing with individuals that aren't reproducing sexually, of course.


Is co-transport within a cell active or passive transport?

Co-transport, also called secondary active transport, is a form of active transport because it is using the energy from one concentration gradient to transport another molecule across the membrane against its concentration gradient. The concentration gradient which drives this process requires energy to set up in the first place, which is why co-transport is considered active.


Why do slime molds pulsate when growing into their fruiting body?

What you have observed is called shuttle streaming. This is how Physarum polycephalum (I assume this is the species of slime mold in the video) and many other slime molds move.
I found this here;

The movement of P. polycephalum is termed shuttle streaming. Shuttle streaming is characterized by the rhythmic back-and-forth flow of the protoplasm; the time interval is approximately two minutes. The forces of the streaming vary for each type of microplasmodium.
The force in amoeboid microplasmodia is generated by contraction and relaxation of a membranous layer probably consisting of actin (type of filament associated with contraction). The filament layer creates a pressure gradient, over which the protoplasm flows within limits of the cell periphery.
The force behind streaming in the dumbbell-shaped microplasmodia is generated by volume changes in both the periphery of the cell and in the invagination system of the cell membrane.


Relationship between action potentials and EEG recordings

Most of the EEG waves are not directly generated by action potential, because it is too short and has a high frequency. They are generated by synaptic activity (overall propagation potential of axons).

The amplitude of this propagation potential depends on the impedance of the brain. Higher impedance means higher amplitude. Impedance is higher for low frequency signals.

The amplitude is also affected by the direction of the EEG vector so parallel axons which go in the same direction should produce a higher wave in amplitude.

Reference: Rudell AP, Fox SE. The propagation potential. An axonal response with implications for scalp-recorded EEG. Biophys. J. 1991 Sep;60(3):556-67. doi: 10.1016/S0006-3495(91)82085-9. PubMed PMID: 1932547.


Spontaneous ringing is caused by When the outer hair cells put energy back into the vibration, which is known as positive feedback. The process is meant to amplify very quiet sounds more so than loud ones. Normally this works, and you would not notice the sound. But occasionally, the amplification level of one or more outer hair cells will go awry and as a result, the whole system will erupt into spontaneous oscillation.

When this occurs, it becomes audible to us. We perceive it as a ringing in the ear, or “sudden-onset ringing tinnitus see here”. As with most of our biological systems, there are quite a few homestatic control mechanisms (negative feedback) which exist to correct the problem and get rid of the oscillation. It takes about 30 seconds for this mechanism to begin, and then sends messages which suppress the ringing. After the message is sent and received, the tinnitus percept begins to fade away.  You can tell when this reaction has taken place as its often accompanied by a slight reduction in hearing sensitivity (like background or ambient noise we hear suddenly getting quieter), followed by a feeling of fullness in the ear. It usually takes about a minute for this process to fully complete.

Sources:

Wikipedia. Wikimedia Foundation. Web. 30 Jan. 2016 (https://en.wikipedia.org/wiki/Tinnitus)
"What Causes Spontaneous Ringing In Our Ears?" Zidbits. Web. 30 Jan. 2016.
"What Causes That Spontaneous Ringing in Your Ears?" Sciencedump. 2015. Web. 30 Jan. 2016.
"Tinnitus." [NIDCD]. Web. 30 Jan. 2016. (http://www.nidcd.nih.gov/health/hearing/pages/tinnitus.aspx)


What are the white eggs growing from a black stem on the Napa cabbage plant?

I'm no expert in slime molds, but your specimens do in fact look a lot like the sporangia, or spore-producing reproductive structures (i.e., fruiting bodies), of a Mycetozoan slime mold in the class Myxogastria.  Physarum and Comatricha are possible candidate genera based on structure of their sporangia that I can find easily online.

See below for an example image:

 Sporangia of Physarum pusillum. Source: Wikimedia

You can see many photos of the white sporangia of Physarum pusillum here and a close-up of the white sporangium of Physarum pseudocolumellatum here

I don't think I can provide a more specific answer given the quality of your photo or my general lack of deeper knowledge of these organisms. Regardless, no quick search for slime-mold infections in plants produced any information regarding slime mold species that regularly grow above-ground on cabbage.

However, I did find this site which suggests that decreasing the moisture or increasing the salinity of the slime mold's environment will cause it to move along...


Why do some women have menstruation-like spotting throughout their pregnancy?

Here are some causes of bleeding during pregnancy:

early pregnancy (first trimester):

implantation bleeding [1]
infection [1]
after intercourse [1]
miscarriage [2]
ectopic pregnancy [2]
cervical changes [3]

second part of pregnancy:

abruptio placentae [1, 2]
placenta previa [1, 2]
miscarriage [2]
vasa previa [2]
preterm labour [1]

References:

American Pregnancy Association. Bleeding During Pregnancy. Available from http://americanpregnancy.org/pregnancycomplications/bleedingduringpreg.html (accessed 29.07.2014)
U.S. National Library of Medicine. A.D.A.M. Medical Encyclopedia. Vaginal bleeding in pregnancy. Available from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0003748/ (accessed 29.07.2014)
WebMD, LLC. Bleeding During Pregnancy. Available from http://www.webmd.com/baby/guide/bleeding-during-pregnancy (accessed 29.07.2014)


Relative microRNA comparison from from TCGA data?

I would be very careful in making such a claim from sequencing data. There are well known biases in sequencing due to things like GC composition and hexamer composition. Because of this, it's possible to compare relative levels of some species across treatments but tricky to do so within a given sample or samples. One way around this is to perform qPCR using absolute quantification on a few samples and then compare that to sequencing results. Granted, you're not going to have the same samples as TCGA or exactly identical library prep, but it'll be a reasonable starting point. You could then use that to calibrate how reliable the relative levels might be within the TCGA dataset.


Meat and mushroom allergies, why are they so rare?

Whilst it is true that animal cells are more like our own, I'm not sure that would be the reason for non-allergic responses. If we take xenografts (transplanting pig organs for example) we see a profound response.

The latter theory of it having a higher mortality is more closer to the truth. Typically we observe that things we are given from childhood causes induction of tolerance (T reg cells). However this occurs best at a young age and if given orally. Peanut allergies for example are incredibly infrequent in Japan for example. Meat is given typically from a young age.

However what about the vegetarian converts or exposure to new foods as you grow older. Well the theory suggested for this are some antigens act to signal the immune system. These proteins are similar to the cell signals our body uses to tell the body there's a fight on, we are being invaded by something dangerous. This causes an immune system reaction to build up, specfically IgE antibodies. Thus on subsequent exposure, the response is stronger due to a preformed response.

Although these are they hypotheses, they're being actively investigated because frankly they can't be that simple. And of course there is conflicting evidence.

Interestingly, I've met a person with mushroom allergy. It does occur. Maybe polymorphisms (slight genetic differences) means someone responds to antigens others don't?


What is the use of male plants in nature?

Pollen, spermatozoid, ovules and bees

The pollen is a coarse substance containing the spermatozoids. Males plant creates these pollens. As bees visit the flowers, the pollen get stuck on their body. When the bee covered with pollen visits female plant, then the pollen may randomly stick onto the female organ. The spermatozoid grow into a tube within this organ and goes to fertilize the ovule.

In short, bees are ...

In other words, you need females for the ovaries, males for the spermatozoids and bees for the delivery services.

Note that bees don't do this delivery services just to be nice with plants. They do so because they get nectar (substance full of sugar) in the flowers.

Reality is more complex and more diverse

Note also, that reality is more complex and more diverse than what I explained. Not all plant species are pollinated by bees. Not all plant species have flowers. Most plant species are hermaphrodite (have male and female flowers or even have male and female organ within the same flower).


There are organisms with anaerobic metabolism that tolerate oxygen: aerotolerant anaerobes.  "Anaerobic" refers to the metabolic system.  You cannot be sure of oxygen tolerance based solely on metabolic system.

Factors influencing the tolerance of anaerobic bacteria to oxygen

Here is why this is a facultative anaerobe.

This organism does not gain weight when denied air.  One concludes its metabolism is less efficient.

  Curiously, the consumption of sugar increases as air is removed from
  the organismʹs enviroment

Anaerobic metabolism uses sugar less efficiently than aerobic metabolism in organisms that can use both methods. This means oxidative metabolism is the preferred method.

So:  this is a facultative anaerobe because it can get by using anaerobic metabolism, but two pieces of information show that for the organism, anaerobic mode is less efficient than aerobic metabolism.  Brewers yeast is such an organism.


Chromosomes are of different size but why do all chromosomes have similar GC percentage?

As @dd3 points out, average GC% indicates a need for stability and coding regions or structural regions of the genome may need to be more stable.  But the largest %GC in genomes are found in thermophiles - organisms which live in high temperature water - in hotsprings and undersea geothermal vents. This review mentions how some thermophiles can be found with 50% GC.  The extreme thermophile Thermus thermophilus can have a GC% content of 69.4%.

But you are asking how does GC content get averaged out over the length of a large genome.  The answer is variation and selection.  When a gene needs to be more stable because of genomic function or because its trying to live in a hotter environment mutations that convert A/T to G/C base pairs will convey an incremental advantage to survival and will tend to be retained in the gene pool as long as no greater disadvantage to the mutation results.  Over time and as the stability creates a greater advantage, GC % will migrate further and further away from the mean.

This works for both thermo-tolerance and because of the biofunctional constraints of being a telomere, centromere or a coding region - stability and coding constraints play against each other to converge on an optimal GC content in any given stretch of the genome.

Conversely most genomes have a GC content below 50% are migrating there because too much stability can have a cost as well.  Breaking up the DNA helix for transcription and other cellular processes must go smoothly as well for example.

Coding regions are significant for bacteria (E coli is 89% coding sequence).  For coding sequences, the genetic code is logically 50% GC on the average, but if you look at the actual codons in the diagram below you will see that except in the case of a single codon case (tryptophan, methionine) the third base always has a GC option, allowing for a GC content in the mid 60 percentiles.  The constraint of allowing coding sequences to freely vary is only an approximation - in some cases substitutions to amino acids with GC rich codons might move the cieling up a bit. And the more frequent amino acids have the possibility of making 2 or 3 bases of their codon GC bases.  Overall it would be remarkable to find a bacteria with GC% greater than 72%.  Mutations and the requirements of proteins being coded for would simply not allow it.

So: over evolutionary periods these GC mutations accumulate where they are helpful, even to the extent of 2/3 of the genome being GC pairs.  The strongest selective force to accumulate a high average GC% for a genome is exposure of the genome itself to a high temperature environment.

Note that this thermo-stability argument doesn't count for many animals because they do regulate their body temperatures.


A 'good' phylogenetic tree would be completely refined, properly binary, have high bootstrap support for all its branches, and reconstruct clades we think exist with high support values.

Generally high support values(there are other methods besides bootstrapping but that is a question for another time) is a measure of a good tree. There are other concerns, for example a tree that has no felsenstein zones is probably better than one that has lots.

We can know a lot more about trees than you suppose, though. Through simulation studies we can create datasets with a known phylogenetic history and then see how well the methods reconstruct the history. There are still problems(errors in the model used, just random error, ILS, HGT, other things) but mostly that kind of study tells us what good phylogenies look like.

It's very easy to generate a lot of different phylogenies. Using different methods, different models or approximation schemes, different genes or sequences from each species, or simply bootstrapping "new" samples from your existing dataset. A phylogeneticist usually has dozens of trees to choose from, which is a sort of crude bootstrap method itself. If trees look similar, they're probably pretty good. If they don't, you have a problem.


How does the cell select where to to make the break on both chromosomes?

There are proteins that direct the selection of a site where a double strand break will be made on one chromatid.

  Crossovers are not randomly distributed: The histone methyltransferase PRDM9 recruits the recombination machinery to genetically determined hotspots in the genome and each incipient crossover somehow inhibits formation of crossovers nearby, a phenomenon called crossover interference. Each chromosome bivalent, including the X-Y body in males, has at least one crossover and this is required for meiosis to proceed correctly.
  Credit; Reactome

.

  Is it based on some attempt to match sequences on the two chromosomes, or purely on distance from the centromere?

The sequences are matched but not as you have assumed. Following the introduction of a double-strand break in one chromosome the regions around the break are processed (by proteins) and these processed ends invade the opposite chromatid. The formation of a Holliday junction follows, these are the "X" structures between strands in the image below, and they requires base-pairing;

Image credit; EMW2012


Why is the origin (patient zero) required to cure a virus?

Nope. This is a total movie fallacy/exaggeration.

How worthwhile it would be to isolate the original strain is debatable, but certainly not necessary for vaccinology purposes.

On one hand, the inital strain might be interesting to study if its an aetiological agent which has never caused human disease before. It would be the first 'snapshot' of the genomics/transcriptomics of an organism/agent which has been able to jump a species barrier perhaps, or has evolved to survive at our body temperature, evade our immunity and so on.

However, as the infection progresses through a population, in order for it to stay infectious, it must by definition have maintained the molecular patterns that permitted it in the first place, so isolation of the 'zero-th', 10th or even 10,000th infection shouldn't make any real difference from a therapeutic standpoint. It may even be the case that as subsequent infection has in effect, passaged, the organism, that the later strains may even be more dangerous than the initial one.


Why doesn't T5 exonuclease have endonuclease activity in Gibson assembly?

The buffer conditions used in the reaction also mitigate against the endonuclease reaction, so it should not be a problem if you stick to the protocols exactly. I've worked on this enzyme since 1988 and was the original "cloner' of the overproducer see http://www.sayers.staff.shef.ac.uk/fen/   for more information on these enzymes
Jon Sayers, University of Sheffield.


Does anyone know good software for producing tanglegrams?

Dendroscope

Using Dendroscope, I opened the provided example file trees.new. This opens a new window with 16 trees in it.

Shift click on the first two trees (Tree1 and Tree2).
Choose Algorithms $\rightarrow$ Tanglegram...
This will compute the tanglegram and open a new window.

At this point, I get:

There is nothing special in the trees.new file, just 16 Newick trees. So it looks like all you need is to have your trees in the same file or use File $\rightarrow$ Add from file.

I think that the tricky part is that your trees have to have the same tip labels, so that they can be lined up optimally. So in your example, Phalacrocorax pygmaeus and Pectinopygus excornis must have been named the same in the original Nexus file and then modified to produce the final figure.

TreeMap 3

TreeMap requires some preliminary setup. Basically you create a Nexus file manually. Using the 4taxonmatch file from the examples, you can get the basic layout. You have a HOST block and a PARASITE block. Within each one of those is a TREE block, which contains the Newick formatted tree.

The RANGE block inside the DISTRIBUTION block contains the mapping table. Here p maps to u, etc. This is the connection between host and parasite.

#NEXUS
BEGIN HOST;
TREE * Host1 = (u, (v, (w, x)));
ENDBLOCK;

BEGIN PARASITE;
TREE * Para1 = (p, (q, (r, s)));
ENDBLOCK;

BEGIN DISTRIBUTION;
RANGE
    p: u,
    q: v,
    r: w,
    s: x
;
END;

In contrast, you get the correctly labelled tree directly. See below.


In practice, do fishes die from old age?

Yes, at least some fishes have intrinsic lifespans and deaths that are related to their own life-history and not to external forces such as predation or disease.

  Fishes show three types of senescence. Lampreys, eels and pacific
  salmon exhibit rapid senescence and sudden death at first spawning.
  The guppy, red panchax, medaka, platyfish, Indian murrel and many
  other teleosts undergo gradual senescence, as observed in most of the
  vertebrates. A number of fishes (e.g. sturgeons, paddlefish, female
  plaice, flatfish, rockfish) show indeterminate growth, the occurrence
  of senescence in them is supposed to be very slow or negligible.

Patnaik BK, N Mahapatro, and BS Jena. 1994. 'Ageing in fishes' Gerontology 40:113-32


What is the name of this green plant with thin leaves?

This is a moss of the genus polytrichum, most likely it is P. commune or P. formosum


The dam methylase has three different functions:

Correction replication errors, since the new DNA molecule
is only hemimethylated (the old strand is methylated, the newly
synthesized is not). Since the proof-reading only takes place on the
new strand, errors introduced during replication can be corrected.
Regulation of replication: The ori of the chromosome is methylated to ensure that is only replicated once.
Regulation of transcription: Methylation of GATC sequences promote the transcription of genes.

For further details see the references.

References:

The great GATC: DNA methylation in E. coli
The dam and dcm strains of Escherichia coli--a review.
Dam methylation: coordinating cellular processes.


Pseudomonas bacteria are generally not difficult to grow:

Rugged and opportunistic, Pseudomonas use a wide range of nutritional sources, even very simple nutritional environments without any organic compounds. - Sigma

For specific species, you'll want to use a selection medium. Sigma-Aldrich has a number of  commercial products for selection and I'm sure you can find a recipe that suits your species with a Google search.

Related reading:
Medium for the Selective Isolation of Members of the Genus Pseudomonas from Natural Habitats (Grant and Holt, 1977)
Evaluation of various selective media for the detection of Pseudomonas species in pasteurized milk (Van Tassell et al., 2012)


For how long would a flu-contaminated parcel be an effective disease vector?

How long should I wait before handling the parcel to avoid contracting the virus?

If you use gloves, or don't touch your face and just wash your hands after opening, you don't have to wait at all.  If you don't use gloves or want to pick your nose, rub your eyes, or fiddle with your beard while opening the package, wait 24 hours if the package is nonporous, and 2 hours if it is not. Generally, whether contaminated or not, don't lick, eat, inhale, or rub your eyes with the package :)

Influenza and similar respiratory viruses are transmitted by large droplets, aerosols, and fomites. Your package is a fomite, an object that can be contaminated and transmit disease. There is some debate about what mode of transmission is most significant for influenza, but fomites definitely do transmit influenza and similar viruses. In a study of homes and daycare centers with children who had an active influenza infection, 59% of home objects that were tested were positive for influenza. It's reasonably likely that your package was, at least at some point, contaminated.

@LDiago's answer is useful here, but deserves some clarification. The UK National Health Services information cited in that answer comes from this seminal study. I'm not entirely happy with the wording on the NHS website, though. Virus survives on nonporous surfaces for 24-48 hours. Virus is transferred from nonporous surfaces to hands in detectable amounts for 24 hours. If your package is paper, the relevant test is transfer from cloth or paper. Virus survives for 8-12 hours, and is measurably transferred to hands after 15 minutes to 2 hours. In any case, virus transferred to hands from a fomite survives for only 5 minutes.

Infection from fomites, however, requires virus to be transferred from the fomite to (typically) the hand, and then from the hand to respiratory tract epithelium. Inoculation of nasal passageways is sufficient for infection in laboratory conditions. Conjunctival and oral inoculation may also play a role. You can read more about this in Cecil Medicine Ch. 372 and Murray Medical Microbiology Ch 59.


The image you used is from a Reddit Thread, where the mushroom is identified to be Cortinarius violaceous. More information on Cortinarius violaceous can be found here.

Although it could be a different mushroom, as the picture you provided is not a picture of the specific mushroom you saw.

Another picture of Cortinarius violaceous

Source: velutipes.com

All credit goes to Reddit user tubergibbosum for the identification.


Black Rhino, status: critically endangered

With around 5000+ black rhinos left in existence, and population numbers seemingly recovering (up from ~2400 in 1995), the black rhino is not really under any immediate threat.* The major threats to black rhinos is poaching (for the rhino horn trade), and, with prices for rhino horn increasing, it looks like it will be a problem for a while to come. Furthermore, corruption, war/civil unrest, easy access to guns, poverty, funding cuts (etc.) contribute to make the battle against poaching more difficult.

African Elephants, status: vulnerable

There are around 470,000 African Elephants left in the wild, and 25-30% of these are the Forest Elephant subspecies, so they aren't going anywhere soon.* Numbers are steadily increasing (~4% per year), although some populations are reducing. Poaching for ivory and bushmeat are signficant problems, but habitat loss and fragmentation is a massive issue. Elephants occupy a large number of habitat types and populations cover vast ranges, it is very difficult to protect an entire population range such that elephants could freely and safely move throughout their range (particularly at national borders), but things are getting better in many cases and efforts are ongoing.

  An increasing number of transboundary elephant populations are co-managed through the collaboration of relevant neighbouring Range States. Large-scale conservation interventions are also planned through the development of conservation and management strategies at the national and regional level.

Polar Bear, status: vulnerable

Population estimates range between 20 and 25 thousand polar bears in the wild, and populations are on the whole fairly stable at the moment (in population studies, for populations where enough data was available, 1 grew, 6 were stable, 3 declined over a 12 year period). These animals are dependent on sea ice which, with human caused climate change, is rapidly declining. Climate change poses a more serious threat to polar bears. Relative to many things, like poaching and habitat fragmentation, it will take a very long time to reverse the tide; it may even be too late to prevent fatal damage to the polar bear habitat. They are also at risk from hunting, pollution, and habitat disturbance. Realistically, it is hard to predict when (or if) polar bears will go extinct because there is so much variance in the prediction of climate change and loss of habitat (sea ice).

Giant Panda, status: endangered

Less than 2000 pandas are left in the wild. Hunting and habitat loss remain to be enormous problems for wild pandas; masses of deforestation and fragmentation is occurring in their range. The chinese government has established >50 panda reserves, but this covers around ~60% of the population. The population trend is a decreasing one, which is serious cause for concern, and fragmentation of populations could reduce genetic diversity (increasing inbreeding depression and reducing adaptive capacity). Despite popular belief, pandas reproduce fairly well in the wild, it is in captivity that we have struggled, and that causes problems for breeding programs that can boost numbers and restore genetic diversity to sub-populations.

Mountain Gorilla, status: endangered

Fewer than 1000 mountain gorillas are left in the wild and populations are declining. Habitat encroachment, deforestation for the charcoal industry, bushmeat, and poaching are major issues affecting populations, and much has been fuelled by conflict (e.g. the 1990's war in Rwanda) in their range (in the last 20 years, 140 Virunga rangers have been killed trying to protect Gorillas). Also affecting them is human disease including the common cold which is often fatal to gorillas.

Bengal Tiger, status: endangered

Currently with a population of >2500, and with populations stabilising, and even rebounding in many areas (I was in Ranthambore last year, numbers have risen from ~20 to ~60 in the last 10 years), it seems the Bengal tiger is no immediate threat of extinction.* The major threats are poaching, population fragmentation, and habitat encroachment which leads to conflict with (and killing by) humans in the areas. Project Tiger is a major programme in India which has greatly contributed to successful growth in tiger numbers. The range of tigers is under increasing pressure from encroachment.

Summary

In summary, few models will be able to predict when or if any of these species will go extinct. Even if the short-term problems can be overcome, loss of genetic diversity prevents issues for the long-term prosperity of these species. Many of the problems are fixable in a relatively short time but will take a lot of effort and money, (such as poaching, hunting, deforestation) because they are mainly about cultural and social issues.

Climate change is perhaps more concerning because reversing the effects of human caused climate change will be extremely difficult (social and economic pressure), and slow to reverse; by the time we reverse the trend of rapidly declining sea ice it may be too late. Therefore, out of your species I'd say it's a close call between polar bears (despite good numbers they perhaps have the worst prospects of rescue) and mountain gorrilas (because numbers are so low and conservation projects are fighting difficult problems such as poverty and the effects of decades of civil wars and unrest). This article from national geographic suggests mountain gorillas may have as little as ten years left, while polar bears may be able to cope with some amount of warming, but the rate of warming is a major concern.** The WWF has also warned that pandas are not far from extinction.

What happens if we lose these species?

Many of these species are very attractive to the general public. The loss of some species would likely be worse than others; many of these are used to promote ecotourism and this would have varying effects for each. For the cases of black rhinos and african elephants many of these areas have many other species which are of interest to ecotourists (lions, leopards, cheetahs, white rhino, giraffe, crocodiles, buffalo, and many other mammals and birds, even sharks). However, if black rhinos went extinct then there would probably be losses in those species too (they face many of the same problems). Ecotoruism in the relevant areas tigers and pandas on the other hand are hugely important draws, India and China simply don't have the same diversity and abundance of highly sought after species with which to boost ecotourism should either go extinct (there are other nice species in these areas, but few are as highly sought as tigers and pandas). It's much the same for mountain gorillas and polar bears, these areas have less to fall back on should their species go extinct, so in many cases these species are of major economic importance.

That said, losing one or two of these species could cause some good. The outrage at losing some of the most popular animals in the world would be enormous. Funding for conservation and social pressure would likely swing massively more in favour of conservation efforts, making the fight to protect other species easier. Personally I don't hope we will ever have to rely on this strategy.

* Relatively speaking

** Strong selection may not get adaptive responses to occur quickly enough because generation times, standing genetic variation etc. such that while populations may adapt they don't adapt quickly enough.


What are reciprocal inhibitory synapses?

It might be better understood if written with a comma as:

  reciprocal, inhibitory synapse

though the rules for this comma usage in English might discourage this because writing "inhibitory reciprocal synapse" doesn't sound quite right. I would say the author wrote it correctly even though it is not perfectly clear.

In this context, they are separate adjectives describing the synapse: inhibitory, because it suppresses firing, and reciprocal because Cell A gives input to Cell B, and Cell B also gives input to Cell A (where Cell A is the amacrine cell and Cell B is the bipolar cell).

The word reciprocal in this context is the adjective definition of the word reciprocal:

  given, felt, or done in return.

Note that it isn't the synapse itself that is reciprocal or in both directions, but that the cells have a reciprocal relationship.


Relationship of the DNA of a eukaryotic gene to the 5'-UTR of its mRNA

Concise Answer

The 5′-UTR region of a eukaryotic mRNA is derived from the RNA transcript of the region of a gene between the transcription start site and the DNA corresponding to the translational initiation codon. It differs from that region of the initial transcript in most cases by having a modified guanosine nucleotide added at the 5′-end in a ‘cap’ structure, and in some cases by lacking an intron present in the former.

The Transcriptional Start Site (TSS) and the Promoter

This answer is in terms of the TSS rather than ‘promoter region’ or ‘promoter sequence’, favoured by the questioner because in eukaryotes, at least, there is no simple and easily definable promoter sequence. A 2012 review of metazoan promoters begins with the definition: “Gene promoters are the loci overlapping transcription start sites (TSSs), at which the total regulatory input of a gene is integrated into the rate of transcriptional initiation. The immediate role of the promoter is to bind and correctly position the transcription initiation complex…”.

A simplified diagram of some components of human promoters (adapted from an earlier review by Hahn) is shown below. The position of ‘Inr’ — the Initiator box which contains the TSS — varies with respect to the TATA box (usually from –25 to –30 in humans),  as does its sequence. Hence, even ignoring the alternative TSSs mentioned by @Luke it is not possible to identify the TSS unequivocally by inspection of the DNA sequence of a gene in the way the questioner would apparently wish.

The Translational Initiation Codon

It should be mentioned that it also not possible to identify the mRNA translational initiation codon unequivocally by inspection of the DNA sequence of a gene. Although 90% or more cases follow Kozak’s rule, so that it corresponds to the first ATG, in some cases it may correspond to the second ATG, and in a small minority — where internal initiation occurs — to some distal ATG. There are also a very few examples of initiation of translation at codons other than AUG.

Introns in 5′-UTR regions of pre-mRNA

A common rationalization of the intron/exon nature of eukaryotic pre-mRNA is in terms of alternative splicing to produce different protein sequences. Perhaps because of this, the presence of introns in the primary transcript containing the 5′- and 3′-UTRs is often ignored (see Bicknell et al. for a review). In fact, approximately 35% of 5′-UTR precursors contain introns, not present in the mature mRNA.

5′-capping of eukaryotic mRNA

The vast majority of eukaryotic mRNAs have a cap at their 5′-end, produced by the addition of a guanosine nucleotide in a 5′-5′ pyrophosphate linkage to the 5′-residue (usually A) of the pre-mRNA. This is subsequently methylated at carbon-7; and 2′-O-methylation of the ribose of the subsequent one or two nucleotides may also occur.

Footnote

Although “DNA makes RNA makes Protein”, I do think it important to describe features of information molecules in terms of their actual composition. Thus, the 5′-UTR has to be defined in terms of mRNA, not promoters or exons. If one makes reference to the information content of DNA or RNA than I think a form of words should be used to make that clear. Muddled forms of words can easily lead to muddled thinking.


Is there a family equivalent to "congener"?

Confamilial is the term for same family, it has even been used in print.

  Congenerics were twice as likely to fight as conspecifics, and confamilial competitors were three times as likely to fight as conspecifics.


Can ants sense food from a long distance?

Ants follow odor cues in the wind.  A study by Wolf and Wehner (2000) manipulated ant antennae and wind direction to show that ants followed odor plumes on the wind. A more recent study by Buehlmann et al. (2014) showed that desert ants of the genus Cataglyphis cued in on linoleic acid, a so-called necromone (death scent) released by dying insects. Here's a popular article that summarizes the latter study.  Chances are good the ants are followed the odor plumes coming from your mostly empty food container.

Literature Cited

Buelhman, C. et al. 2014. Desert ants locate food by combining high sensitivitty to food odors with extensive crosswind runs. Current Biology 24: 960-964.

Wolf, H. and R. Wehner. 2000. Pinpointing food sources: Olfactory and anemotactic orientation in desert ants, Cataglyphis fortis.  Journal of Experimental Biology 203: 857-868.


Alternatives to commercially available flow cytometric analysis software for use in cell cycle analysis?

Sounds like you should look into Bioconductor's flow suite.  I actually really like doing flow analysis in R, but it takes some practice and getting used to.

The biggest problem you will run into (in my opinion) is gating.  It's not easy to setup a GUI point and click gate.  Rather, you'll be more forced and inclined to set limits with algorithms or hard value limits.

I found .Net Bio to be fun, but not nearly as powerful as Bioconductor.

Meta note, couldn't think of a less opinion oriented way to answer other than just to say "It can be done in R utilizing Bioconductor."  If this is still off, I'm fine with deletion.


Can bioluminescence be used for cancer or tumor detection?

Not in human but you can use this technique with genetically modified model organisms as described here.

The procedure is quite simple, you express the luciferase enzyme under the control of a specific promoter (specific for your cell type, like cancer) and provide luciferin via intravascular or intraperitoneal injection. The targeted cell type (for example cancer) will light up.

If you want to use that as a diagnostic tool in human you can't as the organism must express an enzyme catalyzing a bioluminescent reaction. Actually with the advance of genome engineering tools you might be able to do that even in humans (e.g. using CRISP/Cas9).

What is the advantage of bioluminescence over fluorescence? I might be wrong but I don't think there are any. I would rather express a fluorophore rather than an enzyme that requires a substrat.


Why does the affinity of haemoglobin for oxygen decrease at high altitudes?

The answer to this question is yes, a decrease in oxygen affinity will decrease the oxygen taken up by the haemoglobin (Hb), but it is an appropriate response because it will have a greater effect in increasing the release of oxygen to the tissues.

This is not intrinsically obvious. It happens because of the (sigmoid) shape of the oxygen binding curve, and can only really be appreciated if you examine the curves for the normal situation and that in which there is increased 2,3 Bisphosphoglycerate (2,3-BPG) producing the change in oxygen affinity. I have devised a figure to demonstrate this, although it is not based on actual data, so should only be regarded as illustratative.

At sea level the lungs pick up oxygen at 1 (say 100% saturation of
Hb) and when the oxygen pressure drops to 40 mm Hg in the tissues (2)
the Hb will be 55% saturated. Hence in this example they have
released 45% of a full complement of oxygen.
If we look at the same curve for high altitude, in this example the oxygen pressure at the lungs (1') will be such that the Hb is only 80% saturated. Thus at 40 mm Hg in the tissues (2) when Hb is only 55% saturated it will only have released and made available 25% of a full complement of oxygen.
Now consider the effect of high altitude acclimatization with increased 2,3-BPG production changing the equilibrium and the oxygen binding curve (red). At the lungs (3) the Hb will be less charged with oxygen — only 70% saturation — but at 40mm Hg in the tissues (4) it will be much less saturated than on the black curve — 30%. Thus it will have made available 40% of a full complement of oxygen.

This is not a perfect solution, which is why over a longer term there is increased production of red blood cells to provide more haemoglobin to compensate for the smaller amount of oxygen it can bind.


Which hydroxyl from either the phosphate or the glycerol is taken during synthesis of a phospholipid head?

In all phosphorylation reactions, the oxygen of the hydroxyl group in the substrate attacks P of phosphate. This is because of high partial positive charge on P which is bonded to four highly electronegative oxygen atoms. When the bond forms between the substrate oxygen atom and phosphorus of terminal phosphate, electrons are transferred to the O that bridges the ester bond between 2nd and 3rd phosphate. Therefore the O of the substrate is retained and that of the terminal phosphate (of ATP) becomes the part of the 2nd phosphate (now terminal phosphate of ADP).

See this


What is the nesting period of the European Turtle Dove in middle to southern Italy?

I think it would be difficult to answer except people living around or visiting frequently the Naples region as the bird distribution covers the whole central Europe during summer time.

Then my answer will focus more on the italian part.

One interesting reading would be this document from the European Commission.
Disclaimer: this document refers to biological aspects of the turtle dove, but the main topic is the pressure of the hunt on that bird.

In page 10 they mention that:

  Stable populations are found in central Europe: Italy, Austria, The Czech Republic and Slovenia (BirdLife International 2004a).

Page 14 table shows the period of migration and breeding countries (EU 25 only).

And in page 17, they shows that probably between 200'000 to 400'000 breedings pairs are present in the whole Italy (Estimation by Birdlife International)

Here are some refrences:

Breeding and distribution at IUCN
Distribution at avibase

As you can see the distribution os quite large and the figures of estimated breeding pairs very large.

You can also check the observations (not only breeding) with that avibase link.

For the probability to nest the same place, I would say it's possible as in general the birds can go to the same place as the previous year but I cannot say more if the European Turtle Dove have a different behaviour or not. If they have a quiet place where there are no disturbance (Hunting, human activities) or predators, they would probably come back to the same place.


Are there examples of cells with more than one nucleus?

Yes, they are called Multinucleate cells. There are two types of multinucleated cells

Syncytia
Coenocytes

I highly recommend having a look at this answer for the definitions.

Examples of Syncytia include

Osteoclasts
Skeletal muscle fibers (thanks @kmm)

Examples of Coenocytes include

Codium (Thanks @GerardoFurtado; see picture below)
Blastoderms early in the development of a fruit fly

  Are there examples of organisms with multiple nucleuses?

Side note: The plural of nucleus is nuclei

In many fungi, during sexual reproduction, a fusion of cytoplasm happen early in the mycelium but a fusion of the nucleus happens only very late (just before sporulation). This is a type of Coenocytic mycelium. In these species, non-negligible fractions of their cells are multinucleated.

There are endosymbiotic and endoparasitic eukaryotes in other eukaryotes that would result in a cell containing several nuclei but that would not count I would guess as the nuclei belong to different species.

Picture of Codium. The entire algea is a single multinucleated cell.


That is a Nephila clavipes, a.k.a, "golden silk spider". According to Wiki, this is the only golden web-orb species that's indigenous to America.

  Can anyone identify this species of spider and whether or not it is venomous?

"..there is little real danger from an encounter with the golden silk spider. The spider will bite only if held or pinched, and the bite itself will produce only localized pain with a slight redness, which quickly goes away. On the whole, the bite is much less severe than a bee string." (source)


"Synaptic clearance" is referring to the clearing of a neurotransmitter from a synaptic cleft.  A synapse is a place where one neuron can stimulate another neuron. The tiny gap between the neurons is called the synaptic cleft. The presynaptic (stimulating) neuron releases a neurotransmitter (such as dopamine) into the cleft and some of the neurotransmitter is recognized by receptors in the membrane of the postsynaptic (stimulated) neuron.  In order for the synapse to stimulate the postsynaptic neuron a second time, the concentration of the neurotransmitter in the cleft must be reduced to its original levels.  This reduction is called clearance, and can occur in several ways (mainly dependent on the type of neurotransmitter).  The neurotransmitter may be transported back into the presynaptic neuron for reuse; this is called reuptake.  The neurotransmitter may also be degraded (broken down chemically) into an inactive form.  To a lesser extent, neurotransmitter can also be absorbed by astrocytes or simply diffuse away out of the cleft.


I would hardly ever say never where biology is concerned.  In this case that utilizing red rather than blue light for a plant would require many of the basic assumptions of photosynthesis in terrestrial plants to be revised, but since we're talking about another planet, that might not really be an issue.

If we are asking only about how we could change our plants to work with IR light, I'd say that might take a few hundred million years of selection and its harder to imagine.

Firstly photosynthesis in another planet doesn't have to fix carbon or produce oxygen - both of these chemical processes utilize the relatively greater energy produced in blue and red light photosynthesis we see in plants here.

Secondly using IR would have its particular questions associated with it.  In this case the energy quanta are very small and in fact in the same range as chemical bond vibrational energies.  Such energy might be hard to capture with any efficiency since simple heat would tend to compete with the photon, so this would work better if the entire system were at a relatively low temperature.

The leaves could be black or they could be completely clear by the way.


What is the genetic background for fast metabolism?

The expression "fast metabolism" is very general and makes the question hard to answer. I will hence answer in the most general sense possible and then just give one example.

Yes, it is most definitely the case that there is genetic variation underlying the variation in metabolic abilities in the human population (btw, this post summarizing the partitioning of phenotypic variation might be helpful to you). For example, Greenlandic Inuits have a series of mutations that affect their ability to digest polyunsaturated fatty acids allowing them to cope with the impressive amount of animal fat that is/was found in their traditional diet (Fumagalli et al., 2015).