Can virus survive dessication (and come back functional after rewetting)?

Viruses that are protected by a protein shell (non-enveloped) like adenoviruses, rotaviruses, and hepatitis A virus can survive dessication for a while. This paper showed adenovirus remained clinically infectious after 28 days on smooth surfaces, and this paper found around 1% of human rotavirus and hepatitis A virus survived after 60 days.
Other viruses might survive dessication even longer, these are just the ones I looked into.
Regarding rewetting, any test for virus survival will re-wet the virus.


In biradial symmetry, in addition to antero-posterior axis there are also two other axes or planes of symmetry at right angles to it and each other such as the sagittal or median verticular-longitudinal and transverse or cross axes. Such animals have two pairs of symmetrical slides i.e there are two planes of symmetry.

You can visualize it as a combination of radial and bilateral symmetry. The body has similarity on either side of a central axis but slight differences in sections next to each other if divided across any plane.

E.g.ctenophores.

for more info

In this image you can see that there are two planes of symmetry, one passing along the oral-aboral axis and the long axis of the mouth. The other passing along the oral-aboral axis and short axis of the mouth. The antimeres on either side of one plane are slightly different from the antimeres on either side of the plane (Imagine in 3D). The comb plates give it radial symmetry and mesogleal layer (jelly-like) give it bilateral symmetry.

If you are interested in the evolutionary aspect, then read this.


There are are few ways this can be done.

One important example, is case of Phineas Cage who's accident lead to severe brain damage. This changed his behavior, which allowed scientist to connect physiology with behavior. Namely, left frontal lobe damage caused change in personality, without significant change in other important behaviors such as memory.

Same way we can look on naturally occurred brain damage via modern imaging techniques (X-ray, CT, MRI, fMRI) and connect those to behavioral abnormalities.

We can also learn about neural substrate of behavior by experimenting in the lab: by looking at effects of tissue damage. Basically, you ask "what happens if we damage this part of the brain". This way we can figure out parts of brain that regulate different parts of sleep by dissecting animal's brain stem in different regions.

Another option is to "look" at brain while it functions and detect important active regions. Here you can use any number of techniques: fMRI, EEG, direct electrode probing of brain regions, or in animals optical calcium imaging. Point is that in these experiments you ask (or make) your subjects to perform behavior X and see how and where that behavior activates neurons.


Are the Fastq files content is truly random

In my experience, the distribution of reads on the flow-cell is pretty much random, but the sequencing errors are not necessarily randomly distributed.  In all Illumina instruments I have seen, it is common to see edge-effects, or other localities on the flow cell where the error profile differs from the rest of the cell, and QC pipelines generally test for this problem.

A particular issue with the HiSeq3000/4000 patterned flow-cells is that, in situations of under-clustered runs, it would be typical to find the same sequence repeated multiple times in nearby 'clusters' - in other words, a clustering of clusters all containing replicates of the same underlying molecule.  Even for runs where there is no severe under-clustering, it might be expected that duplicates would be found in adjacent cells.  qcfail.com has an outline of this phenomenon: https://sequencing.qcfail.com/technologies/hiseq/


What traits make mountain goats so well adapted to mountain living?

Mountain goats belong to the subfamily Caprinae, or goat-antelopes. The higher family is the Bovidae (cloven-hoofed mammals).
Now members of Caprinae are pretty stocky in their build and have thicker fur both of which help them survive in the higher altitude. Their ability to scale/descend sheer cliffs with such agility comes down to their cloven hooves. Their hooves enable them to grasp onto the the face of the mountain in areas other animals could not as well as shift direction very quickly. Despite the fact that cloven-hooves are not unique to mountain goats or other members of Caprinae it is a trait essential for them to be able to inhabit those harsh environments.

Nubian Ibexes (also a member of subfamily Caprinae) are experts at climbing as well; one of the best Caprinae members in my opinion. Nubian Ibex baby and fox


Why not use Cu(OH)2 as a dye for protein electrophoresis?

Copper hydroxide does not dissolve very well in water, which means you will have trouble soaking them into your gels.

Also, even if you managed to add enough copper hydroxide beforehand (in the wells), it is unlikely that the copper(II) ions, if any existes, will travel along with the protein due to its size. (Copper hydroxide itself does not have any charge.)

As for the paper Stella mentioned, the copper salts are used after electrophoresis to produce a negative image, which is exactly what you cannot do with copper hydroxide.


Is Homo sapiens the only species capable of prioritization?

There is a very simple experiment you can do that will demonstrate that animals prioritize. Give a dog two bones. Preferably one which is more tasty than the other. Say one has more meat on it. The dog cannot eat both at once and you will observe it choosing one over the other. This is a clear example of prioritization.

Again with a dog, try observing one greeting two people it is fond of. If you and a friend stand a few meters apart when the dog comes up to you, the animal will choose to greet one of the humans first. Prioritization.

Any animal, or plant, fungus, bacterium or archaeon for that matter, that is ever presented with a choice between two actions during its lifetime, will have to be able to prioritize in order to chose between them. Clearly they can as our world is not strewn with, for example, panicked, confused looking squirrels trying desperately to chose which tree to climb.


Why didn't these scientists restore electrical activity in this pig's brain?

Restarting electrical activity would mean that at least parts of the brain become active again and possibly restoration of almost all cognitive functions. While this would be a tremendous scientific and medical break-through, it would also mean that effectively locked-in syndrome would have been induced for these pig brains. Therefore just attempting to restore electric activity in isolated brains has huge ethical problems and was for this reason probably not allowed (or ever attempted).

Whether or not it should be allowed to test this in pig brains (in order to learn how to adapt the procedure to humans) is a different question (and not one for this SE) - the best way to go about would probably be to restore electric activity not in isolated brains, but with the brains still in animals.


What is the healing process of mouth wounds?

To build on the answers from @Armatus and @S-Sunil

The healing mechanism involves the inflammatory process, which is the same in almost the entire body. In particular in both skin and mucosa (both referred to as "epithelial" tissues), when there is a break, platelets and clotting factors clot off any bleeding vessels, white blood cells (neutrophils and macrophages in particular) collect and destroy any bacteria, dead cells and muck, and then the process of regeneration occurs (with ongoing inflammation), where stem cells in the surrounding tissue regrow cells, new blood vessels may be formed and scar tissue is laid down to give extra strength. Eventually after these stages of healing, there is "remodelling" where the structure basically gets better.

As to why oral wounds heal quickly and don't get infected that much? There are a bunch of reasons. One is that the head and neck has an excellent blood supply- just think of scalp wounds where you bleed like crazy but then they heal very well. Another is that mucous membranes have immune functions that stop invading microbes. Generally speaking we divide this into "innate" immunity which is a general response, and "adaptive" immunity which is tailored towards specific bugs. The mucosa has both. There are neutrophils and macrophages (innate) which live in that area, there are lymphoid patches (like lymph nodes, and adaptive), there are immunoglobulins specific to mucosa (IgA) which is adaptive in nature, and the epithelial lining cells themselves will signal to the rest of the immune system if there is damage or an infection. Plus, saliva itself has chemicals and enzymes which break down oral bugs.

Most of the oral bacteria themselves are not particularly invasive. Just think, every time you brush your teeth, you cause multiple abrasions in your mouth. In fact, measurable amounts of bacteria from the mouth end up in your bloodstream every time  you brush your teeth! And yet, we don't end up with bloodstream infections as a result. This is partially because the rest of our immune system (and the structure of our heart and vessels) is intact, and partially because oral bacteria are not very invasive or pathogenic. They kind of have a sweet deal living in your mouth minding their own business and not killing their host, and even causing infection in an oral wound would make their continued survival less likely.

In addition I should probably point out that skin has a great deal of bacteria on it as well, and yet we rarely get infections from them (unless colonised by an invasive species), for the same reasons.


First, allow me to provide the link to an old paper that deals with development in Ananas comosus, it should be freely available and answer this question in more detail: http://onlinelibrary.wiley.com/doi/10.1111/j.1469-8137.1936.tb06884.x/pdf

Now, to briefly explain the observation that a mature plant will grow from the region where the leaves of the pineapple attach to the fruit, it should be noted that the pineapple fruit develops at the top of the central stem of the plant in a developmental process known as influorescence (please see a picture of a pineapple plant). Since the top portion of the fruit is in fact the end of the primary stem, this region contains the apical meristem, a collection of stem cells that are apparently is sufficient to give rise to a mature organism. Pineapple development has apparently been a topic of constant research for nearly a century (due to its economic importance), so there are quite a number of papers that can provide much more detail, but many of these are not freely available.

In nature the primary means of pineapple propagation is the formations of lateral shoots, the growth of which consequently are accelerated by influoresence of the main shoot.

Now the actual way the plant grows is not quite as simple to answer, as plant development is often as complicated as animal development, but in general it is a function of cell division and elongation. In the root apical meristem, there is a region known as the quiescent centre which contains the actual root stem cells. Directly behind the quiescent centre is a region known as the merismatic zone, which features extensive cell division, and directly behind that is the elongation region where the cells grow, effectively pushing the root tip through the soil. In the region behind the elongation region, the maturation zone where the cells have reached full length, cells begin to form more rigid cell walls and differentiate into the different tissues of the root.

The shoot apical meristem is dome-shaped, the top of the dome is known as the central zone and is analogous to the quiescent centre of the root apical meristem, the sides of the dome are the peripheral zone, a region of rapidly dividing cells that give rise to the leaves, and the central region of the dome is the rib zone that gives rise to the stem structures. Elongation, differentiation, and maturation also occur below the meristem region, but involve the additional complexities of leaf organogenesis.

There should be considerable additional information on plant development online.


Identify this black dragonfly with a bright bluish-white band around its body

The closest match I can find is Pseudothemis jorina:

It's very similar to your pictures in regards of body shape and the light distinct band, although I'm not sure it would normally be found in Taiwan. It's more common further south like Thailand and Malaysia.


If you have an antigen (something foreign for the immune system, for example a virus or bacteria) this consists of many different epitopes (immunogenic regions), as shown in the figure below (from the German Wikipedia, Antikörper means antibodies). The antigens are taken up by special cells of the immune system and processed to get small peptides:

To produce highly specific antibodies, the body has to undergo a specific immune reaction against these peptides. In the beginning of this reaction antibodies usually have a rather low affinity (bind only weak) against their antigen. This is changed by the so called affinity maturation in which the antibodies are mutated to make a variety of different new antibodies. These are then again "checked" against the antigen and the ones with a higher affinity are positively selected.

So antibodies with a strong binding to their antigen are favoured against such which have a less strong binding which can lead the selection of only a few antibodies, even if a complex antigen which has many immunogenic peptides is used. This is positive in the way that these antibodies are very effective in directing an immune response against the virus/bacteria but can be critical if the pathogen has a high mutation rate as this leads to a pathogen which does not have this antigen anymore.


What exactly makes red meat (probably) unhealthy?

The gut microbiome is partly to blame, at least for the associations of red meat consumption with heart disease.  Red meat has a high concentration of L-carnitine, which is metabolized by bacteria in the gut to produce trimethylamine, which is further metabolized by FMO3 in the liver to produce trimethylamine-N-oxide (TMAO). High blood levels of TMAO are associated with higher risk for both cardiovascular disease and early death from any cause.
Sources on the relationship between the gut microbiome, L-carnitine, and heart health:
New study links L-carnitine in red meat to heart disease
Red meat, TMAO, and your heart

Or is it possible that there is some deep genetic reason why the flesh of mammals is more harmful than the flesh of birds and fish for human consumption?

The NIH gives the following values for the carnitine content of different foods:

Food
Milligrams (mg)

Beef steak, cooked, 4 ounces
56–162

Ground beef, cooked, 4 ounces
87–99

Milk, whole, 1 cup
8

Codfish, cooked, 4 ounces
4–7

Chicken breast, cooked, 4 ounces
3–5

Ice cream, ½ cup
3

Cheese, cheddar, 2 ounces
2

Whole–wheat bread, 2 slices
0.2

Asparagus, cooked, ½ cup
0.1


Do people even notice when insects other than butterflies and beetles go extinct?

I am not aware of a better list, but you are right that (1) many insects have gone extinct recently, and (2) documentation of insect extinction is poor.  An article in Conservation Biology (2005) says

  The biodiversity crisis is undeniably an insect biodiversity crisis. Yet insect conservation remains the awkward “kid sister” to vertebrate conservation. Nowhere is this clearer than in what we know, or rather do not know, about insect extinction, particularly for those extinctions that may have already occurred. ... What accounts for the tens of thousands of expected but undocumented insect extinctions? What does this discrepancy mean? How important is it to our understanding of extinction and the future of ecosystems? These should be questions at the heart of species conservation, yet they have hardly been addressed. No peer-reviewed articles have been published reviewing modern insect extinctions, and no estimates of global extinction rates have explicitly focused on insects.

--Modern Insect Extinctions, the Neglected Majority (my emphases)

The book Insect Conservation Biology (2012) may have more info, though it still seems to focus heavily on the more charismatic species like butterflies.


The effect of depth on net primary production in aquatic ecosystems

After a quick glance at the book "Light and Photosynthesis in Aquatic Ecosystems" by Kirk (2010), I think that the cause for the productivity dip towards the surface partially lies in photoinhibition, due to high light intensities at the surface. Here are a couple of relevant quotes from the book (Google books: p. 371):

  In this light saturated state, the electron transport and/or CO2 fixing enzymes (most likely, the latter) are working as fast as they are capable, and so any additional absorbed quanta are not used for photosynthesis at all. From the end of the linear region through to the light-saturated region ([i.e. close to the surface, my addition]), since photosynthetic rate does not increase in proportion to irradiance, (P/Ed steadily falls, see Fig. 10.3) the quantum yield and conversion efficiency necessarily undergoes a progressive fall in value. This is accentuated further if, at even higher light intensities, photoinhibition sets in. If the cells contain photoprotective carotenoids, in which absorbed light energy is dissipated as heat rather than being transferred to the reaction centre...

However, the suspended bottle methods often used to estimate these depth gradients might be part of the problem, by overestimating the effect of photoinhibition, by forcing plancton to stay at the same depth (p 358):

  Depth profiles of phytoplancton photosynthesis, such as those in Fig. 10.4, determined by the suspended bottle method, tend to overestimate the extent to which photoinhibition diminished primary production. In nature, the phytoplancton are not forced to remain at the same depth for prolonged periods. Some, such as dinoflagellates and blue-green algae, can migrate to a depth where light intensity is more suitable. Even non-motile algae will only remain at the same depth for extended periods under rather still conditions.

I hope I got the quotes right (quick manual retyping). There are many more relevant sections in the book as well, which seems to cover all kinds of aspects of aquatic photosynthetic efficiency and how this can be a function of depth.


Why isn't the insertion of a single nucleotide destructive for DNA?

A single substitution can often be silent, or at least not impact the structure and function of the resulting protein in a significant way. But what you describe is a frameshift, and that is one of the most destructive mutations. It will completely change the sequence of the protein after this mutation and disrupt the function of those parts of the protein.

Insertions or deletions that result in a frameshift are absolutely destructive mutations.


When was the last common ancestor of pig and human?

Last common ancestor is about 97.5 Million Years Ago.

TimeTree.org Pig vs. Human

That being said, they are close enough to us that they are a vector for influenza viruses that are able to make the jump to human pretty easily.

Also we use their tissue as a homologue for human in forensic research. We also use valves from pig hearts to replace defective human valves.

This Nature News Article reviews some of the work being done with Pig to Human Tissue Transplantation. Though granted the methods they are looking at rely heavily on targeted gene editing.


It is a Burmese brown mountain tortoise - Manouria Emys Emys
 I differentiated it from a burmese black mountain turtle by this method.


How can I measure the population growth of yeast?

The standard way to measure growth in a liquid culture is to measure the optical density (OD) of the solution – basically, how cloudy it is. Bacteria or yeast in a solution will absorb light that passes through it, making it more cloudy (or turbid). Within a certain range of turbidity, the OD of the solution is directly proportional to the concentration of organisms in the solution, and you can use it to accurately estimate the population in your sample. Outside of this range, you'll need to accurately dilute your sample to get it into this linear range.

Generally, we use a spectrophotometer to measure absorbance of red-orange light (this is called OD 600, for optical density for light with a wavelength of 600nm). A google search turns up a number of plans to make cheap, homemade spectrophotometers that could let you take these measurements without having access to a lab, though I can't speak to how accurate they may be. You might also look at home-brewing supplies, as brewers are also interested in measuring yeast growth and tend to have lower budgets than molecular biologists.

You only need a spectrophotometer that uses visible light to measure bacterial/yeast growth. Many specs also work in the UV spectrum which allows them to measure DNA concentration, but you won't need that.


Try looking for "Luer valves" or "Luer fittings".

For instance, we buy this kind of supplies from WPI.


To quickly answer your question, yes DNA changes over the life time of many organisms including humans.  You have a whole host of mechanisms in your body that try to prevent your DNA from changing, but they are not perfect.

A good example of this is DNA degradation due to aging.  When discussing aging in biology, we use the technical term senescence.  Of interest here is the shortening of telomeres due to mistakes made in your cells as they continue to divide (copying the DNA to each new daughter cell).

In a grown adult, there's not some master well of DNA somewhere such that if you change it there it will immediately change the DNA throughout your body.  Most of the cells in your body have DNA in them (red blood cells are just one example of cells that don't have DNA in the traditional sense). Most of these cells can and will divide over time (mitosis) to produce new cells with copies of that DNA.  However, there are also plenty of cells that don't divide often or at all in healthy adults.  If one is concerned about schizophrenia, it would be important to note that many neurons in the CNS are in this group of static cells.

Considering environmental effects, there are plenty of things that can change your DNA. Radiation, gamma and x-rays in particular, do a great job of disrupting, degrading, and occasionally mutating DNA.  The class of chemicals and physical agents that can change DNA are called mutagens.  This shares a root with the verb mutate, which is when something is acting on genetic material to cause it change.

You will note that I said genetic material, and not DNA.  Without getting too far into the debate of what is "alive," DNA is most certainly not the only "construction protocol" for earthly organisms.  RNA is one common alternative, but there are weirder ones that are hard to describe like prions.


Why do we need two markers to measure a recombination rate?

If at least one locus is homozygous

If a recombination event happens between two loci where at least one is homozygous, then you would not see anything. Consider for example the following strand sequences in a diploid individual

-----A-----B----
-----a-----B----

Whether a recombination event occurs or not, the two possible chromosomes passed down to an offspring are

-----A-----B----
-----a-----B----

Therefore, you cannot tell whether recombination has occurred.

If both loci are heterozygous

Now consider the following individual

-----A-----B----
-----a-----b----

If no recombination event has occurred between the two loci of interest then the two possible chromosomes that will be passed down are

-----A-----B----
-----a-----b----

If on the other hand a recombination event has occurred between the two loci of interest then the two possible chromosomes that will be passed down are

-----A-----b----
-----a-----B----

Therefore, you can tell whether a recombination has occurred or not.


It seems very feasible to synthesize human DNA (please inform my
  ignorance, if I'm wrong. lol.) and it looks very promising after
  reading this:
  https://www.wired.com/story/live-forever-synthetic-human-genome/.

It is certainly possible to synthesize human DNA, but it's another thing to create a functional chromosome. In fact, in the article you link to, they are discussing a research effort to synthesize a human Y chromosome. As far as I can tell they haven't actually done this yet, they are just proposing to attempt it. George Church is a highly regarded genomicist, but the article is very sloppy about distinguishing what they think they can do from what they've actually done. There has been work with human artificial chromosomes (HAC), but these have been special purpose constructs that successfully replicate and divide in cells, but don't duplicate an entire natural chromosome.

Synthesizing a human genome would just be the start of the therapeutic process. You then face the question of how to place the synthesized genome in the cells of the recipient. Current approaches to gene therapy involve inserting a single "repaired" gene into a virus, and then infecting the relevant tissue with that virus. This doesn't insert the gene into all cells of the body, just the ones infected with the virus. For some simple genetic diseases this is enough to relieve the symptoms of disease. You can't insert an entire human genome into a virus though.

It's also been proposed to harvest stem cells from the recipient, modify them with the repaired gene, and re-insert them in the diseased tissue. Again this would affect only a portion of a single tissue, not all the cells of the body. It's also one thing to insert a short sequence into a stem cell, but nobody knows if you could swap out a stem cell's entire genome and still maintain it as a stem cell. Also, this would only work for tissues that are still actively dividing. Many important tissues (in the brain for example) have stopped dividing or divide only slowly in adults.

Even gene therapy involving single genes has been approved in only a handful of diseases. It's sill almost entirely experimental. What you are suggesting is still in the realm of wild speculation. Speculation can be inspiring and motivates research programs, but don't starting counting chickens yet.


Highest Pressure Human Body Can Survive In?

The deepest recorded simulated dive is still the on-shore French Hydra 10 experiment at 701 msw (meters salt water); at a pressure of 71 atm. Since breathing a mixture containing helium is required at such depths (to avoid the extreme narcosis produced by nitrogen at such depths), the new problem helium causes is

  High-pressure nervous syndrome (HPNS). HPNS, brought on by breathing helium under extreme pressure causes tremors, myoclonic jerking, somnolence, EEG changes, visual disturbance, nausea, dizziness, and decreased mental performance. Symptoms of HPNS are exacerbated by rapid compression, a feature common to ultra-deep "bounce" dives.

Actually that Wikipedia description is a bit misleading, the problem is caused by any gas mixture, not just helium, but other gasses like nitrogen or hydrogen have a narcotic effect that counteracts HPNS. HPNS sets in at about 120m:

  The high pressure
  neurological syndrome (HPNS) begins to show signs at about 1.3 MPa (120 m) and its effects intensify at greater depths.
  HPNS starts with tremor at the distal extremities, nausea, or moderate psychomotor and cognitive disturbances. More severe
  consequences are proximal tremor, vomit, hyperreflexia, sleepiness, and psychomotor or cognitive compromise. Fasciculations
  and myoclonia may occur during severe HPNS. Extreme cases may show psychosis bouts, and focalized or generalized
  convulsive seizures. Electrophysiological studies during HPNS display an EEG characterized by reduction of high frequency
  activity (alpha and beta waves) and increased slow activity, modification of evoked potentials of various modalities (auditory,
  visual, somatosensory), reduced nerve conduction velocity and changes in latency. Studies using experimental animals have
  shown that these signs and symptoms are progressive and directly dependent on the pressure. HPNS features at neuronal and
  network levels are depression of synaptic transmission and paradoxical hyperexcitability.

The problem with extreme helim pressure was partially alleviated in the Hydra experiments by mixing/replacing some of it with hydrogen, in the so-called Hydreliox mixture.

  For the Hydra VIII mission at 50 atmospheres of ambient pressure, the mixture used was 49% hydrogen, 50.2% helium, and 0.8% oxygen.

The French did this based on prior experiments which found that the narcotic effect of hydrogen reduces HPNS (or even completely eliminates it at lower depths):

  A H2-He-O2 mixture with 54 to 56% hydrogen was studied with 6 subjects (professional divers) during 2 dives to 450 m. The 38-h compression was the same as that used with other types of breathing mixtures (He-O2 and He-N2-O2). The results obtained during compression and during the stay at 450 m in H2-He-O2 show that the EEG changes (increase of theta activities in the anterior regions of the skull, decrease of alpha activities) are similar to those found with other respiratory mixtures. On the other hand, the other symptoms of high pressure neurologic syndrome (HPNS) were clearly improved for the same depths. Thus, neurologic symptoms (tremor, dysmetria, myoclonia, drowsiness) are nonexistent, and the performances during psychometric tests remain similar to those of the surface. Hydrogen, with its narcotic potency, suppresses some symptoms of HPNS and seems to open new perspectives for deep diving.

Of course, having hydrogen (in such large proportion) and oxygen in a gas mixture poses dangers of fire, explosion etc. This is avoided by decreasing the oxygen concentration; alas this cannot be a one-step process (for diving):

  The major problem with hydrogen-oxygen mixtures is the potential for explosion. Although the concentration of oxygen needed for combustion of oxygen-hydrogen mixes varies a bit with pressure, a general rule of thumb is that hydrogen-oxygen mixes above 5 %  O2 are at-risk.. So, to avoid nasty fires and explosions, hydrogen is only considered as a breathing gas component at pressures where a less-than 5% oxygen concentration in the breathing gas mix gives a partial pressure of oxygen great enough to sustain life. Perhaps the most common example of a hydrogen-fire related disaster is the destruction of the Hindenburg dirigible. [...]

  In 1944 Arne Zetterstrom discovered a way to breach the transition between compressed air and Hydrox without risking explosion. The technique was to descend to 100 feet and switch to a 4% oxygen / 96 % nitrogen mixture. After breathing this mix for sufficient time to allow the oxygen concentration in the lungs to drop below the "explosion threshold," the diver switched to Hydrox and continued descent. On ascent, the diver again used the Nitrox (4% O2 / 96% N2) as a transition between Hydrox and air. Using this technique, he descended to 363 feet. At that depth, the alteration in voice characteristics, coupled with excitement, made communication impossible and additional dives used a telegraph key.  [...]

  During the mid 1960's research into the use of hydrogen in breathing gases resumed with animals breathing Hydrox for up to 24 hours at 70 Ata. One interesting aspect of the animal research was the suggestion that hydrogen reduced the HPNS (high pressure nervous syndrome) often observed with helium based gas mixes on deep dives. Ultimately animals would be taken to 3500 feet on hydrox.

  In 1983 COMEX, the French deep diving concern (perhaps more famous in the US as the company providing the submersible used in the recovery of artifacts from the Titanic) began a series of dives to investigate the narcotic potential of hydrogen. Divers including H.G. DeLauze, President of COMEX, descended in open sea to approximately 300 feet for five minutes. The divers could not perceive a difference between Hydox and Heliox at that depth.  Chamber dives to 300 m (984 ft) demonstrated that hydrogen possessed a narcotic effect different from nitrogen. Hydrogen narcosis (the "hydrogen effect") had a tendency to be more psychotropic, i.e. more like LSD, while nitrogen narcosis had an effect similar to alcohol. This deeper work suggested that Hydrox as a binary gas mix would not be too useful at depths below about 500 feet.

Based on that COMEX developed a protocol of switching from heliox to hydreliox at 250msw.

A more recent (1994) COMEX paper reported that at 500m (on hydreliox), manual dexterity was about 80% of the surface one, while the arithmetic ability decreased to 60%. So not dying and being able to function as on the surface, aren't the same thing.

Also these experiments are time consuming and costly. In Hydra VIII, the whole thing took one month, of which only 10 days or so were spent at maximum depth. And in case "something bad happens" interventions aren't easy in such settings.

A 1984 American experiment with trimix at 650m was aborted after one of the three subjects (despite negative previous neuropsychiatric screening, as well having substantial commercial diving experience and successfully taking part in the previous experiments of the series) developed hallucinations and then full blown mania at 625-650m.

  The Atlantis IV dive was designed to test the ability of 5%
  N2 trimix breathing mixture (5% N2, 0.5 atmosphere
  oxygen, with the balance helium) to counteract the
  [high pressure nervous] syndrome without nitrogen narcosis. [...]

  The dive began with an initial compression rate of
  30 m/hour to 300 m (1000 ft) sea water equivalent
  pressure. By day 3 of the dive, at about 470 m, subject
  C had developed significant insomnia. On day 4 (540
  m), this subject became stressed and complained of
  mild auditory illusions of music and visual distortions
  consisting of a “halo effect” around the chamber’s
  apparatus. On day 5 (625 m) of the dive, the subject’s
  irritability, insomnia, and agitation worsened. He was medicated with temazepam, 60 mg, and achieved
  substantial relief of these symptoms after 15 hours’
  sleep. However, with further compression to 650 m,
  subject C experienced a recrudescence of auditory and
  visual illusions and developed rapid speech, racing
  thoughts, shortened attention span, and difficulty in
  focusing on tasks. Ankle clonus, marked hyperreflexia,
  and myoclonic jerking were documented, and he complained of nausea and weakness. In contrast, the other
  two subjects performed normally in almost all respects.
  On day 9 (650 m), the subject stated he felt “paranoid”
  and that he felt like “I’m going insane.” He
  began to carry a mirror to look at himself to “remind
  myself that I’m not a raving maniac.” He stated that
  colors were enhanced and vivid and he could see
  “unusual” mosaic patterns on the metalwork within
  the chamber. He was unable to comply with instructions
  to enable cognitive function to be tested because
  of extreme agitation and distractibility.[...]

  Early on day 9 (650 m), the decision was made to
  halt the dive, but decompression from 650 m is still
  experimental and could not be accelerated. Because the
  decompression process was expected to last as long as 30 days, it was necessary to consider medicating the
  subject more intensively. Since lithium had been shown
  to exacerbate symptoms of the high pressure nervous
  syndrome in animals and the effects of phenothiazines
  at such high pressures were virtually unknown,
  the decision was made to control the diver’s agitation
  with benzodiazepines. Accordingly, diazepam was used in doses up to 120 mg/day. This treatment only
  mildly sedated the subject and provided no real control
  of his behavior.
  The subject’s agitation persisted over the next 14
  days and was marked by decrements in his cognitive
  function and bursts of aggressive paranoia, grandiosity,
  and irritability. By day 24 of the dive (383 m), the
  subject’s irritable and aggressive behavior was becoming
  potentially dangerous and led to the decision to
  medicate with chlorpromazine, up to 300 mg/day.
  Within 48 hours of the beginning of chlorpromazine
  treatment there was dramatic improvement in the
  subject’s behavior. He became relatively calm and
  better organized. He denied having illusions or hallucinations. [...]

  Ten days after exiting the chamber, the subject again
  exhibited signs of hypomania including hyperactivity,
  insomnia, and irritability. Lithium carbonate therapy
  lessened these symptoms and was continued prophylactically
  for 6 months. It was then discontinued
  without any recurrence of symptoms.


How different are these terms: Phylloclade, Phyllode, Cladophyll and Cladode?

Apart from the discrepancy of the cladophyll term I can say that both your teacher and the wiki page are correct.

If you read the Wiki page carefully it states that

  Phylloclades and cladodes are flattened, photosynthetic shoots, which are usually considered to be modified branches. The two terms are used either differently or interchangeably by different authors.

(As you have also quoted)

This is simple because both phylloclades and cladodes are stem modification for photosynthesis and xerophytic adaptation as well. So in this context they are interchangeable

Also if you have further read the article it states why the terms are interchangeable and why not. The different levels of definition are given:

  Definitions of the terms "phylloclade" and "cladode" vary. All agree that they are flattened structures that are photosynthetic and resemble leaf-like branches.

  one definition, phylloclades are a subset of cladodes, namely those that greatly resemble or perform the function of leaves,[2] as in Butcher's broom (Ruscus aculeatus) as well as Phyllanthus and some Asparagus species.

The definition given by your teacher can be interpreted by these two definitions stated in the Wiki page:

  By an alternative definition, cladodes are distinguished by their limited growth and that they involve only one or two internodes.[3] By this definition, some of the most leaf-like structures are cladodes, rather than phylloclades. By that definition, Phyllanthus has phylloclades, but Ruscus and Asparagus have cladodes.

  Another definition uses "phylloclade" to refer a portion of a leaf-like stem or branch with multiple nodes and internodes, and "cladode" for a single internode of a phylloclade.

But phyllode is a leaf modification, specifically a modification of the petiole for photosynthesis and a xerophytic adaptation to some extent. (Source is the Wiki page itself)

So to conclude

phyllode is completely different from phylloclade and cladodes.
Taking the type of morphology of the plant into consideration and the definition used, phylloclade and cladodes may be used interchangeably or may not be.


Are brassica oleracea cultivars the same species?

Cultivars are, per definition, the same species of plants. Animal breeds are the same species too, think of the bewildering phenotypical variety of dogs for example; they are still the same species, i.e., Canis lupus.

To your question - Yes, cabbage, broccoli, cauliflower, and Brussels sprouts are the same species.

Hybrids of these plants are called cultivars; broccoli and cauliflower yields broccoflower for example. However, I wasn't able to find evidence of a hybrid between cabbage and cauliflower - a cabbaflower?


Equation you have mentioned is balanced chemical equation. In reality these are series of Redox reactions, major two as follows,

Oxidation of oxygen from water in presence of light (energy from photon),

$ 2H_2O  \xrightarrow{Photons} O_2 + 4H^*$

Ions produced from above reaction reduces carbon dioxide ,

$4H^* + CO_2 \rightarrow (CH_2O) + H_2O$

So both equations combined, we can write general form as

$nCO_2 + nH_2O \xrightarrow{Photons} (CH_2O)n + nO_2$

In simple words to answer your doubt, in final equation 2 oxygen molecule coming from per 2 $H_2O$ molecules and 1 coming from per $CO_2$ molecule. Hence final balanced equation is

$6CO_2 + 6H_2O \xrightarrow{Photons} 6(CH_2O) + 6O_2$


Why do humans circulate monosaccharides instead of disaccharides as in plants?

One of the reasons could be  -

  humans and many other animals have active circulatory systems,
  there is little need for targeting sugars for specific parts of the
  body. The entire body would rapidly reach equilibrium with the glucose
  level of the bloodstream, and thus there likely never evolved the need
  to target specific organs to receive sugars via disaccharides

Source : This

Other reason could be that disaccharides are harder to transfer inside the cells than monosaccharides.


I just want to understand WHY brain cells .... are okay with aneuploidy

Great question. The standard hypothesis has been that aneuploidy confers some kind of advantage to  the function of the organ (brain). After initial reports estimated a very high (>30% of brain cells) aneuploidy, it would be plausible that any potential negative effect would somehow have to be compensated. One hypothesis was that it increases the functional diversity of the neurons.

However, this notion is outdated. For instance, a recent study, which also nicely summarizes preceding literature, and has been published by Knouse et al. PNAS 2014 ( http://www.pnas.org/content/111/37/13409.full ), and has applied a more sensitive and accurate measurement, and also surveyed other tissues, found that the fraction of aneuploid cells in the brain is around 1-2%, and not higher than in most other tissues. One possible conclusion, which has also been drawn by the authors, is that for the brain aneuploidy is as much of a problem as for other organs, and that - given the low fraction of aneuploid cells, which is similar to other tissues - aneuploid cells in the brain do not contribute to some special organ-specific property. (Concerning your related questions to brain: the aneuploidy in brain is believed to result from cell division artifacts - also see paper mentioned above.)

  I just want to understand WHY ... plant cells are okay with aneuploidy

Although plants appear more tolerant against aneuploidy than humans, aneuploidy can be quite harmful to them, and can easily lead to phenotypic aberrations. While the basis of the increased resistance of plants over humans isn't known, or at least hasn't been known at the time of the publication listed below, it appears linked to some genetic factors as different strains can have a different robustness - see Henry et al. , Genetics, 2010 ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998307/ )

  Is aneuploidy/aneusomy only a problem for cell division?

No, aneuploidy can create further problems (e.g.: also see second paper). For instance, in plants, it can also change the activity of genes, or the spatial organization of chromosomes - as described in Huettel et al. Plos Genetics, 2008 ( http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1000226 )


Ways to identify/distinguish individual coyotes?

The Wikipedia entry for subspecies of coyotes has a very useful chart here (click [show]) that gives a description, range, and other information for each of the 19 subspecies of coyotes. Since I presume you are from the California area, I would focus on the descriptions of coyote subspecies that could exist around your area, such as the San Pedro Martir coyote, which has "reddish summer fur and a short, broad skull" to differentiate among the various coyotes you many encounter. Generally, the coyotes differ in color, teeth, tail size, fur, ears, and other such factors. As for determining if you've seen a coyote already, I suppose there's no real way of knowing unless there is a unique marker on the coyote's fur or appendages that differentiates itself from the others; however, examining the coyote's scats and comparing them may be a viable option for this, but that would require you to examine close to the coyotes rather than from afar.


How does human life expectancy change with age?

I think you might be looking for period life tables

  A period life table is based on the mortality experience of a population during a relatively short period of time. Here we present the 2014 period life table for the Social Security area population. For this table, the period life expectancy at a given age is the average remaining number of years expected prior to death for a person at that exact age, born on January 1, using the mortality rates for 2014 over the course of his or her remaining life.


Is it dangerous to eat a mutated eggplant descended from a radioactive ancestor?

While it's always possible that a mutated eggplant will produce a new toxin, this is very unlikely. I don't know how much higher the mutation rate is near Fukushima than in general but the difference can't be huge. Even if it's, say, 5 or 10 times higher than normal (I'm making up these numbers), the risk is still tiny. Actually, plant breeders sometimes use radiation to produce more variety to work with and we don't worry about that.


I think a key factor is that DNA molecules are not passive bits of string that are left to move freely (which is what causes knots in string-like things that are left alone too long).
For one thing the DNA molecule is an active part of the cell metabolism, as it is constantly being transcribed (to generate RNA and proteins) or copied or corrected and so on. And as part of its role in metabolism the DNA molecule is closely associated with RNA molecules, proteins and specifically proteins that the DNA is wrapped around called "histones". The Wikipedia page for "Chromatin" (what chromosomes are made of, basically) describes various aspects of this organization, including:

That DNA which codes genes that are actively transcribed ("turned on") is more loosely packaged and associated with RNA polymerases (referred to as euchromatin) while that DNA which codes inactive genes ("turned off") is more condensed and associated with structural proteins (heterochromatin).

So DNA is constantly being manipulated by all kinds of proteins and enzymes that affect its shape and position in space; it isn't just lying there. And insofar as it might get into knots, that would likely be part of the manipulations of the enzymes and proteins, or would fairly easily be dealt with by them. This doesn't mean DNA doesn't have knots however, in fact it appears it very much can:
DNA AND KNOT THEORY (from The Institute for Environmental Modelling at the University of Tennessee)

Conclusions: Principles of topology give cell biologists a quantitative, powerful, and invariant way to measure properties of DNA. Principles of knot theory have helped elucidate the mechanisms by which enzymes unpack DNA. Additionally, topological methods have been influential in determining the left handed winding of DNA around histones. Measuring changes in crossing number have also been instrumental in understanding the termination of DNA replication and the role of enzymes in recombination.

(note this paper looks at DNA in E.coli, which does not organize its DNA in chromatin the way Eukaryotes do).
Untangling DNA (from the Nature blog CreatureCast, 2013)
This link includes a video about topoisomerases, enzymes also referred to in the previous link that unentangle DNA.
A Monte Carlo Study of Knots in Long Double-Stranded DNA Chains (PLOS Computational Biology, 2016)
Quote from the abstract:

Even though our coarse-grained model is only based on experimental knotting probabilities of short DNA strands, it reproduces the correct persistence length of DNA. This indicates that knots are not only a fine gauge for structural properties, but a promising tool for the design of polymer models.

The active site of the SET domain is constructed on a knot (Nature Structural Biology, 200)
A knot or not a knot? SETting the record ‘straight’ on proteins (Computational Biology and Chemistry, 2003)
These papers discuss potential knots within a histone protein, not DNA, but illustrates that topology and knots can be important in macromolecules:

A knot within the SET domain helps form the methyltransferase active site, where AdoHcy binds and lysine methylation is likely to occur.
A novel knot found in the SET domain is examined in the light of five recent crystal structures and their descriptions in the literature. Using the algorithm of Taylor it was established that the backbone chain does not form a true knot.

Discovery of a predicted DNA knot substantiates a model for site-specific recombination (Science, 1985)
This link is a bit painful to read (and from 1985 so I don't know if it was superseded, but it has over 200 citations) so I will leave it at the title.
And finally this article, which I looked at last but probably should have looked at first because the first sentence of the abstract literally answers your question :
Direct observation of DNA knots using a solid-state nanopore (Nature Nanotechnology, 2016)

Long DNA molecules can self-entangle into knots. Experimental techniques for observing such DNA knots (primarily gel electrophoresis) are limited to bulk methods and circular molecules below 10 kilobase pairs in length. Here, we show that solid-state nanopores can be used to directly observe individual knots in both linear and circular single DNA molecules of arbitrary length.


Why is selection less effective in small populations than in larger?

This question seems to be about negative/purifying selection, judging by the wikipedia quote. Positive selection can often (but not always) occur more slowly in smaller populations, but 'efficiency/effectiveness' of selection generally means the rate at which deleterious variants are purged from the population, so I'll skip out taking about positive selection (unless you did mean that).
First, genetic drift: Genetic drift is the stochastic change in allele frequencies caused by random differences in the survival of different individuals. For example, a mouse might get struck by lightning and not transmit any of its genes to the next generation. Whether or not it was struck by lightning probably wasn't related to its fitness, it was just 'bad luck'. As population size increases, genetic drift becomes weaker because the larger the population, the smaller the proportional impact of each random event that concerns just one individual
Negative selection tends to be less effective in smaller populations because random fluctuations in allele frequency (drift) may lead to deleterious alleles reaching higher frequency. The rate at which deleterious alleles are removed from a population depends on mutation, dominance, linkage, and demography and can vary across populations. Therefore, the average fitness over time may become reduced. Kimura in 1963 was one of the first people to show this.
In reality, 'low efficiency of selection' and 'strong drift' in small populations are the same thing.


How do trees communicate in the "Wood Wide Web"?

I have to say: when you claim that "trees communicate with each other through electrical impulses sent through their roots", you're thinking about Avatar.

Joking apart, what you call wood wide web is the mycorrhizal network.

Mycorrhizal fungi are well known to botanists and ecologists. They are the fungal partner in the mycorrhiza, which is a symbiotic association between a fungus and a plant.

Mycorrhizal hyphae (white) in a root

The novelty about this mycorrhizal network is that, as it was demonstrated, plants can use it to exchange some chemical substances. And, in certain cases, this exchange can be used to improve disease resistance.

However, there is no electrical impulse in this process.

According to Song et al. (2010):

  In theory, plants can also communicate with each other through underground common mycorrhizal networks (CMNs) that interconnect roots of multiple plants. However, until now research focused on plant-to-plant carbon nutrient movement and there is no evidence that defense signals can be exchanged through such mycorrhizal hyphal networks. Here, we show that CMNs mediate plant-plant communication between healthy plants and pathogen-infected tomato plants (Lycopersicon esculentum Mill.). After establishment of CMNs with the arbuscular mycorrhizal fungus Glomus mosseae between tomato plants, inoculation of ‘donor’ plants with the pathogen Alternaria solani led to increases in disease resistance.

This other research demonstrate that the mycorrhizal network can be used to warn neighbouring plants of aphid attacks (Babikova et al., 2013):

  Here, we show that mycorrhizal mycelia can also act as a conduit for signalling between plants, acting as an early warning system for herbivore attack. Insect herbivory causes systemic changes in the production of plant volatiles, particularly methyl salicylate, making bean plants, Vicia faba, repellent to aphids but attractive to aphid enemies such as parasitoids. We demonstrate that these effects can also occur in aphid-free plants but only when they are connected to aphid-infested plants via a common mycorrhizal mycelial network. This underground messaging system allows neighbouring plants to invoke herbivore defences before attack.

In both cases the mycorrhizal networks play an important role in exchanging chemical substances among the plants.

The network has a dark side too: it can be used to deliver allelochemicals from one plant to another, greatly increasing allelopathy. According to Barto et al. (2011):

  Common mycorrhizal networks (CMNs) form belowground networks that interconnect multiple plant species; yet these networks are typically ignored in studies of allelopathy. We tested the hypothesis that CMNs facilitate transport of allelochemicals from supplier to target plants, thereby affecting allelopathic interactions.

Finally: don't rely on media to get scientific information, specially in these times of alternative facts. Sometimes you can get good information in the media, but good and accurate information is way harder to find (an example is this BBC page about the mycorrhizal network). However, in defense of that page in The New Yorker, there is no mention to electrical impulses.

Sources:

Song, Y., Zeng, R., Xu, J., Li, J., Shen, X. and Yihdego, W. (2010). Interplant Communication of Tomato Plants through Underground Common Mycorrhizal Networks. PLoS ONE, 5(10), p.e13324.
Babikova, Z., Gilbert, L., Bruce, T., Birkett, M., Caulfield, J., Woodcock, C., Pickett, J. and Johnson, D. (2013). Underground signals carried through common mycelial networks warn neighbouring plants of aphid attack. Ecology Letters, 16(7), pp.835-843.
Barto, E., Hilker, M., Müller, F., Mohney, B., Weidenhamer, J. and Rillig, M. (2011). The Fungal Fast Lane: Common Mycorrhizal Networks Extend Bioactive Zones of Allelochemicals in Soils. PLoS ONE, 6(11), p.e27195.


Which Enzymes are Responsible for the Biodegradation of Beta-endorphin?

As far as I have been able to find out, there isn't a definitive answer to this question.

β endorphin is a peptide, and it would seem that there are numerous brain peptidase enzymes that are implicated in the hydrolysis of β endorphin and other peptide neurotransmitters. These include aminopeptidase N, membrane-dipeptidase A, angiotensin-converting enzyme and neutral endopeptidase (also called enkephalinase).

For an early (1984) review of this topic see here; there doesn't seem to be a more up-to-date review, but there is quite a bit of literature on the effects of inhibitors of these various enzymes.


What is rotational diffusion and lateral diffusion in plasma membrane?

From this paper, rotational diffusion describes the movement of a membrane lipid around its axis that is perpendicular to the plane of the bilayer, analogous to a person spinning around while standing up.

Lateral diffusion describes the movement of membrane lipids exchanging places with each other across a face of the bilayer, rather like two dancers spinning about their mutual center of gravity.


The reproduction patterns of fungi: what’s the difference between them?

Cell division

Cell division is the process by which one cell becomes two. If we consider multicellular fungi, cell division happens whenever the fungi grows by one more cell. Cell division allows the growth of the organism. Cell division does not necessarily contribute into making a new multicellular organism.

Fragmentation

Fragmentation is a type of non-sexual reproduction. An organism gets split ("intentionally" or "unintentionally") and the different fragments develop into independent mature organisms. Sometimes, on fragment is small than the other one, so that one fragment can be seen as the "parent" and the other one as the "offspring".

Budding

Budding is a type of reproduction by fragmentation, where the splitting occurs due to a specific developmental pathway and not through some external environmental cause (such as getting cut in two by a researcher's knife, a falling tree or the bite of a predator). In other words, in budding, the splitting is "intentional".

More information

wikipedia > Cell Division
wikipedia > Fragmentation (reproduction)

P.S. You won't need to know this biology stuff to get a good score at your TOEFL. On an unrelated personal note, I found this exam particularly unpleasant when I had to take it. Especially when we have to converse with a microphone while somehow ignoring the accents and english mistakes your neighbours are making while talking into their respective microphones. Good luck for your exam by the way :)


Book on the history of Darwin's discoveries and development of his theory

I'm not certain it fills every element of your question, but I really enjoyed Michael Ruse's "The Darwinian Revolution: Science Red in Tooth and Claw."

It's especially good for setting up the collection of worldviews that predated Darwin, and the influence on him by both biologists/anatomists as well as very crucially geologists like Charles Lyell (Darwin really thought of himself more as a geologist; the long time prior to publishing Origin was largely because he was trying to build up some scientific chops as a biologist).

The aspect it is most likely to lack is references to original source material from Darwin. While it certainly draws on such writings, I don't recall it actually containing reproductions of those writings, at least not on a substantial basis.

Importantly, however, this book is not a biography - it is a history of the scientific community at the time, centered around Darwin and Origin and placing them in relevant context.


Is plaque formed even if you do not eat anything?

But I always assumed that plaque is formed by food remains in the mouth

It's not surprising that you'd have this assumption. The clinical term, dental plaque, refers to soft deposits on the teeth. While is often described to the lay public in connection to eating (without brushing), it is not food, or the remains of food, it is a biofilm. Biofilms are complex masses of bacterial colonies in a gel-like matrix produced by those same colonies. The matrix typically, helps the colonies adhere to some surface and protects them from external threats.
Good supporting electronic references of what, exactly, a dental biofilm is and how it impacts the health of your mouth and body are behind a paywall, but you may be able to access them at your local public or school library. Socransky and Haffajee have a good review in Periodontology. You can find it on Pubmed (behind a paywall).
As you suspected, not eating does not prevent plaque formation, but it is not because your teeth are excreting sticky toxins. Your mouth is full of bacteria, most of which lives peacefully without causing any problems. They're the ones that make the plaque, and they will make it whether you eat or don't. Whether or not those bacteria are more likely to cause problems (e.g., cavities and gum disease) if you fast is a question for future research.
There is some evidence that the bacterial composition in the mouse gut changes when they fast, and that obesity is associated with periodontal disease in humans. There is some interesting evidence in support of effects of intermittent fasting that would make it reasonable to ask a research question about the impact on dental caries and periodontal disease, but that evidence isn't enough to support fasting as a treatment for any disease.
tl;dr
Plaque is (caused by) bacteria, not food. It's produced whether you eat or not. Fasting is certainly not an approved treatment for periodontal disease or cavities, and I'm not aware of any direct evidence supporting it.


Could not fit in a comment...

This post (and the excellent answer from Richard Smith-Unna) lists the species that have the smallest genome that we are aware of in different clades.

Yes we can/could sequence these tiny genomes and try to understand what each sequence does. I think that to understand the minimum requirements for life you will mostly be interested in theoretical cytology and synthetic biology than in sequencing simple genomes.

Note that the basic requirement really depends on how you define life. Is a virus alive although it has no metabolism? Would a self-replicating RNA be a living thing? Because we were able to artificially synthesize self-replicating RNA. While the subject is interesting, the main issue is a purely philosophical one: How do you define life?


Is it more likely to develop a throat-ache at night?

It's because your mouth and tongue are stationary at night, so you don't move the slowly-drying saliva around to lubricate tissues. The mucous tissues dry out, resulting in greater friction with muscle movements (like swallowing), and your body is slightly dehydrated after 6-10 hours without water. If you've ever undergone surgery where they intubated you (stuck a tube down your throat to ensure air supply), afterwards it's a very similar feeling to waking up with a soar throat because your throat dries up and the anesthesia prevents muscle movements.

Your immune system actually works better at night and requires rest to work efficiently. Bacteria and viruses don't really care about the time of day, although the muscles of the larynx do ensure that the mucous layer is continuously circulated. The continual circulation helps prevent debris and bacteria/virii from establishing themselves, although the magnitude of the effect isn't on the same scale of other tactics taken by your body.

Several factors can affect mucous/phlegm/saliva production - including infections, hydration levels, environmental temperature, smoking habits, diet, environmental humidity, and lots more. If it's a constant trouble, you can try drinking more water during the day, a steam humidifier, or talking to your doctor.


Perhaps your confusion will be helped by separating for you 2 processes that occur in both skeletal and cardiac muscle contraction.  The first process is the electrical change (action potential) in the muscle cells membrane that triggers the contraction and the second is the contraction of the muscle cell itself.

The latter process, contraction of the muscle cell, is basically the same for both muscle types.  Simplistically this requires high intracellular Ca in both skeletal and cardiac muscle.  In short, when the intracellular Ca in the cell is high all muscle cells will contract and when it decreases they will relax.

The difference between the cell types is what triggers this increase in intracellular Ca when the cells are stimulated I.e. what causes the increase in intracellular Ca.  In skeletal muscles the action potential moving through structures called t tubules directly causes release of Ca from the sarcoplasmic reticulum.  In cardiac muscle this is different as the action potential here causes Ca to enter the cell from outside and it is this small amount of Ca coming from the extracellular space that triggers release of the far larger amounts of Ca in the cell that are needed for contraction.  This is called Ca Induced Ca Release or CICR.

Schematic pictures are the best way to understand the differences in the processes in the 2 muscle types so try these 2 links (Cardiac (https://courses.lumenlearning.com/boundless-ap/chapter/cardiac-muscle-tissue/) & Skeletal (https://opentextbc.ca/anatomyandphysiology/chapter/10-3-muscle-fiber-contraction-and-relaxation/)

You can also access the Textbook of Medical Physiology by Guyton and Hall online or at a school/university library which will give you more detail.


In a Sanger sequencing, what would be happen if different DNA sequence binds to same primer? And how this situation avoided if problematic?

Yes, this can happen if you are not checking your primers against the reference sequences.
Your PCR is done from two different pieces of DNA leading to two sets of chain-terminated fluorescence marked DNA. This leads to superimposed sequences, which looks like this and where you cannot differentiate, which sequence belongs to which strain (image taken from here):

It is problematic, the solution is to design new primers (which are located slightly outside the old target sequence) which only bind to one specific sequence. You cannot purify only one product, as you cannot discriminate between the two.


Do mycorrhiza only form with angiosperm?

Mycorrhiza refers to any fungi that forms a symbiotic relationship with a plant. There are many different species, and they are necessary for healthy plant growth in ~70%-80% of vascular plant species with representatives from more than ~90% of plant families. Needless to say, mycorrhiza associations with plants are very common.

What you may be thinking of is rhizobia, which are not as ubiquitous.  Rhyzobia are soil bacteria associated with legumes (peas, soybeans, clover, lentils, etc.). Rhizobia fix nitrogen for the legume, and the legume forms root nodules where the rhizobia live. The nodules provide an ideal location for the rhizobia to live and thrive. This relationship has only been observed in legumes (scientific name: Fabaceae).

In summary:
Both mycorrhiza and rhizobia form Symbiotic relationships with plants. Mycorrhiza are fungus that form relationships with most species of plants. Rhizobia are bacteria that form relationships only with plants in the legume family.


DNA methylation on the forward vs reverse strand?

In most tissues, close to 100% of DNA methylation occurs at CpG sites. This provides a straightforward mechanism for epigenetic inheritance. Since C and G are complementary, both strands have the CpG site at the same locus and methylation is either present on both strands or on neither. During replication, each daughter DNA molecule inherits a parent strand with the (un)methylated CpG sites. Enzymes can recognise when there is asymmetrical CpG methylation and subsequently methylate the new strand where required. So, for CpG sites, both strands are methylated or not.

In embryonic and induced stem cells, however, ~25% of the total methylation occurs at non-CpG sites (especially CpA). Thus, methylation at a specific locus would only occur on one strand. As far as I know, how/if this methylation pattern is inherited has not yet been elucidated. Furthermore, this type of methylation occurs throughout the chromosome and is particularly high in exons whereas CpG methylation generally occurs upstream of a transcription start site.


Why do we squint when tasting very sour things?

Short answer
Adverse stimuli in general are accompanied by contraction of facial muscles. It is part of our repertoire of emotional expressions.

Background
A disgusted expression and the expression of pain are both accompanied by squinting. Disgusting stimuli include your example of a sour taste, but also include other adverse tastes (bitter) or visual stimuli such as a gross-looking objects. In other words, squinting is likely a common way of expressing adverse stimuli. So the "sour look" may not be easily explained on its own. Instead, it is part of a huge emotional expressive repertoire that makes us human beings. To be able to read these expressions allows us to be empathetic towards others. People with autism and Asperger's syndrome may not be able to do so and are disadvantaged in their social behaviors.

To illustrate the commonalities between sour (#1), disgust (#2) and pain (#3) I would like to share the following web finds.

Sour taste. Source: Getty Images

!
Disgust. Source: Berkeley Emotional IQ test

Pain. Source: Berkeley Emotional IQ test

PS: I am not a psychologist - Consider my contribution as an educated guess.


Should there be separate Ramachandran plots for an amino acid in different contexts?

The phi and psi dihedrals describe the dihedral on both sides of the c-alpha of a single amino acid, and do not involve any angles of the neighboring amino acid.

The Ramachandran plot is something generated from a set of protein structures, an empirical data set. The top graph represents the dihedrals found for all non-glycine residues in a set of structures. You can filter this for proline only, and you'd get the bottom graph. The top cloud of dihedrals represents those found in beta-sheets, and the bottom cloud those for alpha-helices. Sequence (the amino acid before or after) doesn't really matter that much for what's allowed (although we cannot directly deduce this from the data in those graphs).

If you look a little bit more into the structure of helices and sheets you'll also find out why that's the case. In beta sheets the sidechain of the +1 residue is pointing completely the other way, and also in helices there's little interaction between the sidechains of subsequent residues. Secondary structures are built using the amides, not with the sidechains.


Staining cells for FACS at 4 degrees or ambient temperature

You have several questions, please try to limit your posts to one question each. That being said, I'll try to address each of your concerns.

  Does the cold cause these cells to apoptose?

No. The purpose of staining at 4°C and washing with cold buffer is twofold - to maintain viability (all cellular processes slow down at lower temps) and to prevent receptor internalization. This second point is especially critical as you're using a primary and conjugated secondary, which I really wouldn't recommend for sorting unless absolutely necessary, for example if the antibody you're using isn't available in a directly-conjugated format.

  One thing I can do to minimize cell death is do a live/dead stain (we just added that capability).

Live/dead stains are generally a good idea, but make sure the stain you're using isn't cytotoxic. L/D should always be the last staining step before running your samples. A better way (if your sorter supports it) is to use forward scatter (FSC) and side scatter (SSC) height and area measurements to discriminate single, appropriately-sized cells, then gate on them first before gating on your antibody stain (FITC or PE or whatever your secondary is).

  The other thing I read was to use 50% FBS in your collection tube.

I'm not sure how much that will help, especially 293s, which are pretty tough. Just make sure you're diluting the collected cells enough in medium to bring the serum percentage back down to 10%.

  if we are doing many sorts, then some of the tubes may be sitting in sorting buffer for a long time in the queue. How long is too long?

As long as your samples are kept in the dark on ice or at 4°C, they should be fine for several hours at least (I wouldn't go overnight, though). Also, make sure your collection medium is chilled, as it can shock the cells to go from 4° to 37° too rapidly. Collect your sample, plate it, then put it at room temp or in the incubator (depending on your workflow) and let it warm up that way.

  Lastly, we use puromycin and blasticidin as selection markers for our libraries and we usually add these right to the sort after we replate. Should we wait a while?

Nah, don't worry about it. You can wait if you want, or add it right away - I would lean towards adding it more quickly than not, so you don't give unwanted cells any chance of growing out.


What is the best way to clean plastic flasks that have been used for cell cultures - is virkon a good idea?

I use virkon for cell cultures, but for viruses I tended to use standard bleach during the time I worked in a virology lab.


Since the pBR322 is derived from the pMB1 plasmid (which is closely related to the ColE1 plasmid, it does indeed contain the coding information for the rop gene. It's expression will limit the copy numbers from the plasmid, so if you are looking for high copy numbers, the usage of a plasmid without the rop gene should be preferred.

If it is only for the yield in a plasmid preparation, you could also simply scale up your production and make a midi prep instead of a mini or a maxi instead of a midi. It also depends, what you are planning with the plasmid. For cloning purposes mini preps with pBR322 have always given enough yield for me.


Why does ionizing radiation cause only DNA double strand breaks?

Ionizing radiation does cause single-strand breaks and other kinds of DNA lesions that are not double-strand breaks.  However, double-strand breaks are the most difficult to repair and are thus the most likely DNA damage type to result in mutation and / or cell death.  See Fig 1. from DNA damage response signaling pathways and targets for radiotherapy sensitization in cancer:

DNA damage induced by ionizing radiation. The major types of DNA damage induced by IR include base and sugar damage, single-strand breaks, double-strand breaks, clustered DNA damage, and covalent intrastrand or interstrand crosslinking


Experimental Analysis: What are possible reasons for this increase in N₂O production?

This may have no correlation to your project but many insecticides, bacteriocides, and herbicides need a "solvent" or "transfer medium" such as water to be effective. Even when using ethanol in the laboratory against a variety of bacteria 100% ethanol becomes almost ineffective.

I would take a look at running round-up again by itself versus 95% roundup 5% water, and 90% roundup and 10% water and I am sure you may seem some results that will aid your experiment.

Good Luck!


I think that using NCBI Gene would be a better option here:

Go to NCBI Gene http://www.ncbi.nlm.nih.gov/gene/
Enter your gene of interest, in this case CNGA3 (and optionally the species)
Click the species of interest (I'm assuming you are looking for human, the first search result)
On the information page scroll down and click on FASTA which will provide the sequence for the gene of interest.


You need to look up polytene (giant) chromosomes.

  Polytene chromosomes are over-sized chromosomes which have developed from standard chromosomes and are commonly found in the salivary glands of Drosophila melanogaster. Specialized cells undergo repeated rounds of DNA replication without cell division (endomitosis), to increase cell volume, forming a giant polytene chromosome. Polytene chromosomes form when multiple rounds of replication produce many sister chromatids that remain synapsed together.

You can read more about it at wikipedia (http://en.wikipedia.org/wiki/Polytene_chromosome)


Is there any evidence that humans have faced extinction before?

There is ample genetic evidence for a population bottleneck following the out-of-Africa migration. This would account for the reduced genetic diversity found in non-African populations.

There is further evidence for an earlier major bottleneck that reduced the human population to around 10,000 individuals.

These kinds of studies are typically done now via Coalescent theory using whole-genome sequences.

I just found this nice blog post summarizing the Nature paper I linked to.


Can diploidy evolve in absence of sexual reproduction?

I can only offer a partial answer on the theoretical aspects. I don't know if you are familiar with the mid-90s papers by Otto et al. (Otto & Goldstein,1992, Otto & Marks, 1996), but these are definately relevant to your question. They deal with the "masking hypothesis" of diploidy, i.e. that deleterious mutations can be masked by "healthy" alleles, and the trade-offs between diploidy (ploidy level), recombination rate and purging of deleterious alleles. Otto & Goldstein (1992) shows that recombination is essential for the evolution of diploidy, and without recombination haploids will "win" over diploids.

Otto & Marks (1996) is a fairly comprehensive paper that builds on the previous one, and looks at how different mating systems interacts with recombination and purging to influence the evolution of ploidy levels. As a general results they predict a correlation between mating system and ploidy level, with sexual reproduction favoring diploidy while asexual reproduction favors haploidy. However, from what I can see after a quick re-read, there is nothing that prohibits asexually reproducing species to be diploid (and vice-versa) - see e.g. page 206 - and the paper includes a condition that must hold for diploids to invade in asexually reproducing or selfing populations. I have not followed this literature closely though, and I imagine that tracing recent papers that cite Otto & Marks (1996) can be useful to find further relevant studies.

You should also consider that ploidy levels can differ between sexes (e.g. bees), which can lead to antagonistic selection which can influence ploidy evolution (see e.g. Immler & Otto, 2014).

As for the empirical evidence part, I do not have any good examples. However, I imagine that it can be extremely difficult to prove that a lineage have only reproduced asexually (or never asexually), since these things are hard to track in fossils. Also consider that it is common to have both sexual and asexual stages, and many species can have a long asexual diploid stage followed by a shorter sexual haploid stage. From what I know, this is the norm in e.g. algae (arguably a group of fairly "basal" taxa). However, I don't know what the ancestral state of algae was (i.e. if they became diploid before having a sexual stage).

As for the ancestral state of eukaryotes, there seems to be evidence that the ancestral state was in fact facultatively sexual (Dacks & Roger, 1999), which would invalidate your assumption. However, this is only based on a couple of quick literature searches on my part, and I am in no way an expert in this area. There are probably more recent studies on this topic as well. However, it is clear that you cannot blindly assume that eukaryotic haploid is ancestral.


I came across a nice Master's thesis that investigated precisely that. The conclusion reads as follows:

  Automated microbroth dilution-based testing methods are increasingly used by many
  clinical microbiology laboratories to determinate antimicrobial susceptibility. Thus, it is vital that
  these methods are able to accurately determine the correct antibiotic susceptibility patterns of
  microorganisms being tested. In our laboratory, we use the Trek Sensititre system (Well Plate Method). However, if
  this system cannot accurately detect resistance visualized as inner colonies on the Kirby Bauer
  Assay, then the clinical importance of the Trek Sensititre may be called into question.

  Our study showed that the Trek Sensititre was unable to detect the
  additional resistance of inner colonies that are detected using the
  Kirby Bauer Assay. Nevertheless, there are a number of important
  limitations associated with the study: Firstly, the inner colonies
  used in the study were pooled from all inner colonies from the Kirby
  Bauer plate. Because the colonies were pooled, in some cases from
  different antibiotic zones, it is possible that a mixed population of
  resistant organisms that were selected for by the different
  antibiotics were tested. This possible mixture of multiple different
  subpopulations may make the results difficult to interpret. Secondly,
  some inner colonies were selected from antibiotics that do not have
  any CLSI- 47 approved interpretations and would be considered
  inappropriate to report. For example, some Pseudomonas aeruginosa
  isolates displayed inner colonies to ertapenem, an antibiotic that has
  no CLSI interpretations and a drug that would not be used clinically.
  The Trek Sensititre results from those inner colonies showed
  additional issues with multiple different antibiotics. Clinically, the
  patient would not have been treated with that antibiotic, so that this
  resistant set of subpopulations may not have been selected for. Thus
  the results from the study may not be clinically significant but it
  does open up questions to the possibility that the Trek Sensititre may
  not detect clinically significant resistant subpopulations.

  Given that
  the Trek Sensititre can miss resistant subpopulations in Gram negative
  bacilli, it is important to establish the clinical relevance of this
  finding. If the inner colonies selected for by each of the antibiotic
  discs was sub-cultured individually instead of pooled together and
  then run on the Trek Sensititre, then the following results may
  possibly differ from the pooled inner colonies. An important future
  direction would be to determine whether the unreported resistance from
  the organisms in the study had an effect on patient care however, this
  was beyond the scope of this thesis study. Thus, the clinical
  significance of this study’s findings require future study.
  Nevertheless, laboratories should be aware of the potential for
  missing sub-populations of antimicrobial resistant organisms using
  broth-based microdilution methods.


Does denaturing proteins lead to loss of epitopes?

Many but not all B cell epitopes will be destroyed by denaturing.  Those that are conformational will be destroyed, but there are also many B cell epitopes that are linear, based on amino acid sequence only without strong conformation dependence.

Also, depending on your IHC protocol, there's often a fixation step that involves a certain amount of denaturation, though rarely as drastic as in immunoblotting.  Conversely, some proteins are capable of at least some restoration of native conformation after they bind to your blotting substrate.

Bottom line, it's unpredictable, but it works often enough to make it worth trying.


programmatic fast search of 100-1000 short reads to a public server and obtain list of nearby genes

This can be done offline and wont require too much of computational resource.

What you will need:

A fast short read aligner such as STAR or even bowtie (STAR is faster)
Genome sequence (you will have to build index for the genome for your aligner)
A GTF annotations file (get it from GENCODE or any other standard genome repository for your organism of interest)

Before you align remove redundant reads. Keep their counts if necessary.
Align the reads using any of these aligners and obtain the alignment co-ordinates. The default output is SAM format for STAR and a tabular format for bowtie (bowtie also gives SAM).

Column-3 of SAM shows the name of the reference sequence
where alignment happened (chromosome)
Column-4 is sequence start
Column-10 is read sequence. Add the length of this to column 4 value to get stop site.

The columns are tab separated

Now define a window that you define as proximal/nearby (lets say 500nt).

Now all you have to do is find genes that lie $\pm500nt$ from your start/stop sites. In your reference GTF parse for the lines that have the feature "gene".

I am giving an example using awk. You can use any programming language you are comfortable with. Check the GTF format also.

Assuming that you made a file (reads.txt) from your SAM output in this format:

Chromosome <tab> Orientation (+/-) <tab> Start <tab> Stop

I am giving an example awk script:

example.awk

#!/bin/gawk

BEGIN{FS=OFS="\t"}

NR==FNR{
    a[$1 FS $2][$3 FS $4] # store the co-ordinate information from your reads file
    next
}

$3=="gene" && ($4 FS $7) in a{ # quick parse for reference chromosome and orientation

    i=$4 FS $7
    for(j in a[i]){
        split(j,jj,FS)
        if(jj[1]>=$4 && jj[2]<=$5)
            print $0";contained"

        else if($4<=jj[2]+500 || $5>=jj[1]-500)
            print $0";partial overlap/proximal"
        }
}

call it like this:

awk -f example.awk reads.txt annotations.gtf

NOTE: In the above script I have not considered antisense proximity. If you want to allow that then don't parse for orientation. Also gawk version < 4.0 doesn't allow multidimensional arrays. So install gawk>=4.0

The output is by default a GTF because you are printing selected lines of the reference GTF.


Do metastatic cells still have their parent's identity?

Welcome to stack. This is a good question.

To answer your question: Generally, yes.

Howeve like @user137 stated below it can depend on many factors most notably how many division cycles they go through, and also where they metastasize to. The immediate environment of a cell is very effective at altering gene expression.

I use Hepg2 cells regularly. These are hepatocellular carcinoma cells that can be cultured. These cells are known to express 3-hydroxy-3-methylglutaryl-CoA reductase and hepatic triglyceride lipase, two enzymes characteristically highly expressed in liver cells. If we want to do a quick quality control typing we will perform rtPCR for those enzymes. I have seen the expression drop off after about 4 months (~35 passages).

Looking at gene expression (ideally through microarray) is a very valid way to identify/type a cells tissue of origin.


Why does B12 deficiency enlarge red blood cells?

@SPr has given you a good reference in his answer. I thought I'd add some context to it.

The basic problem here is that red blood cells need B12 in order to synthesize DNA. Red blood cells live for about 4 months, and have to constantly be replaced, so when you have a problem with B12, this is one of the cell populations that will be affected. The problem here is actually the anemia. It's not that the cells are too big, but that there aren't enough of them (see the linked reference, as well as Robbins and Cotran Pathologic Basis of Disease, Ch 13, subsection "Anemias of Diminished Erythropoiesis"). The size itself helps identify why there aren't enough of them, distinguishing this anemia from other anemias that cause cells that are smaller than normal.

The mechanism in lay terms (which hasn't entirely been worked out, again, see both the article and Robbins), is that a problem with DNA synthesis causes the cells get larger before they divide. So you have fewer, larger cells. Because it's a universal problem with DNA synthesis, red blood cells aren't the only cells affected.


Short answer: Only some stages of plasmodium are motile.  These use "gliding motility".

Gliding motility relies on actin filaments, which enable the organism to deform it's shape, facilitating movement.

This video provides a good visual representation of the filament-based motility.

  "Gametocytes develop into gametes in the insect midgut, and then fertilize each other to form motile zygotes, which escape the gut."

The ookinete and sporozoite are motile.  The merozoite is non-motile.

Then of course there is the circulatory system of the host.

Source:

https://en.wikipedia.org/wiki/Plasmodium
http://www.sciencedirect.com/science/article/pii/S0092867400812817


I am not an expert on gene guns but I will try to give my answer on this question anyway.

Price-wise they are both relatively cheap. The electroporators consumables are only the cuvettes, they cost 5-10 dollar/each. The gene guns use microbeads as bullets and depending on the material they cost between 200 and 300 dollars per microgram, 10-50 dollars per shot, a bit more expensive than electroporation.

About the organisms, guns are used mostly for plant-cells and few other "hard to electroporate" organisms. I don'd have a proper list of them but roughly, if you work with bacteria, yeasts and mammalian cells, then go for an electroporator.
If you need to work with tissues or entire organisms like worm/insects/plants then go for a gun, you definitely cannot electroporate a leaf. But in general, check the literature on what is currently the best method to transfect your system of choice.

Efficacy, also in this case it depends form the cells you are working with. Electroporation reach 10^9/10^10 transform ants per microgram of DNA in case of E.coli and this is the best efficiency you can get nowadays. All other cells will be transfected at lower efficiency, how much lower? It depends from the cells!

Easy of use. They are both very easy to use, it is matter of pressing a button. For the electroporation you need to prepare electrocompetent cells, but the procedure is very easy. For the gene guns you need to coat the beads with DNA, also very easy.

Maintenance. The electroporator do not need any maintenance at all while the gun may need some care in the long run since it has pumps and pressurised chambers, this stuff usually need some attention but nothing special.

Some references:

bio-rad.com/LifeScience/pdf/Bulletin_9541.pdf

bio-rad.com/webroot/web/pdf/lsr/literature/4006174B.pdf

bio-rad.com/webroot/web/pdf/lsr/literature/4006217A.pdf


What are the allowed evolution operators (on protein encoding sequences)?

The most frequent mechanisms are

Intragenic mutations: when existing genes mutate modifying gene function.
Gene duplication: leads to related genes in a single cell. A gene duplicates and then as two copies are available, one is free to change
Segment shuffling: leads to hybridisation of different DNA segments.
Horizontal transfer is transfer of DNA from one cell to another
Transduction: infection of cells by viruses or other intracellular pathogens where their DNA can integrate into the genome

You are incorrect to say all evolution occurs due to duplication. Your follow up questions are too vague. Genes can become larger or smaller, but yes as they increase so does their diversity.


Are there examples of animals being sexually attracted to another species more than to their own?

Here are a few examples. All are open to debate as to whether it answers your question.

Zoophilia in humans

When asking of example of a "species" that does something, it is easy to forget about the diversity of behaviours among individuals of that species. It raises the question of how frequent must the behaviour be in that species to accept that the species is representative of this specific behaviour. Many might be tempted to disregard humans as examples thinking that zoophilia (sexual fixation of a human on non-human animals) is very rare but the reality appears quite different.

The Kinsey reports (1953) estimated that 8% of men and 3.6% for women had sexual interaction with animals at some point in their lives. More recent studies tend to find somewhat similar results (of the order of a few percents). These numbers seem to go way higher for people living near farms. Although these numbers seem debated, the Kinsey reports (1953) estimated that 40–50% of people living near farms have had sexual interaction with animals at some point in their lives.

Given the prevalence of zoophilia, I would argue that humans could be considered an example of a species where (some) individuals are sexually attracted to individuals of another species.

Many animals have sex with about anything

In my life I have seen many dogs, rabbits and bulls attempt to have sex with inanimate objects. If a dog can be sexually aroused by a pillow (poor pillow), then I am pretty sure it can be sexually aroused by individual of another species.

Here is a picture of a moose trying to mate with a statue of a bison

Note btw that I am talking here about animal species that have a very high cognition, so below is a funny example with a beetle.

A tragic love story

In Australia, a species of Buprestidae (family of beetles) called Julodimorpha bakewelli has gone through an important decrease in population size. The blame is on people throwing their empty bottles of beers on the side of the road. Why? Males are attracted by the brown shiny color of the females and it turns out that many glass beer bottles have this same exact color. Hence, males started to spend all their time mating with beer bottles rather than with females causing a decrease in the species population size.

Sure a beer bottle in not another species but it shows how individuals of a species can be more aroused by something else than individuals of its own species (and the example is funny; the study won the IgNobel prize in 2011).

Amazon Molly

The Amazon molly is a fish species in which there is no males. All Amazon mollies are females. However, the amazon mollies need sperm to reproduce. How is it possible?

The females have to seek for sperm in a sister species in order to activate the development of the eggs. They mate with males of this sister species but don't use the genetic material of the father from the sister species (otherwise they would not be two different species). The amazon mollies are therefore only sexually aroused by individuals of another species. See Kokko et al. (2008).


I agree with your reasoning! If the two genes are perfectly linked, then the answer is $\frac{1}{8}$. If they are perfectly unlinked, then the answer is $\frac{1}{16}$. The answer therefore must be somewhere between $\frac{1}{8}$ and $\frac{1}{16}$.  Good job!

Of course the answer e) is pretty silly as any other answer ('a','b','c' and 'd') would yield to 'e' being necessarily true. So, if you have to choose only one, I would just go with 'd' and highlight that the answer 'e' is silly.

  I still don’t understand how if the two are completely linked, the answer would be 1/8.

Let's consider that at both loci, we have two alleles A and B. Here is a representation of the first F1 individual

-------A----A-----
-------B----B-----

Here is a representation of the second F1 individual

-------A----A-----
-------B----B-----

Of course, they are the same as the parental lines are pure breed. Now, if the two loci are perfectly linked, then the offspring can have the following possible genotypes

-------A----A-----
-------A----A-----,

-------B----B-----
-------A----A-----,

-------A----A-----
-------B----B-----

or

-------B----B-----
-------B----B-----

, but the offspring cannot be

-------B----A-----
-------B----B-----

or an other combination requiring recombination between the two loci. Therefore the probability to be heterozygote for the F2 at two perfectly linked loci is the same as the probability to be heterozygote at one of these two loci (if we assume the mutation rate is negligible).

  Why can't parents be: parent1: -------B----A----- -------A----B----- parent2: -------A----A----- -------B----B-----[?]

Because parental lines are pure lines. When we talk about an F1 generation, we talk about the hybrid between two pure line. By pure line, we mean that we got rid of all genetic variance. So, one parental line is fixed for the A alleles and the other line is fixed for the B alleles.  In other words here are the genotypes of the pure parental lines.

-------A----A-----
-------A----A-----

and

-------B----B-----
-------B----B-----

One parent can therefore only give

-------A----A-----

while the other one can only give

-------B----B-----

so, the F1 generation is therefore necessarily heterozygote at all loci.


What's the highest temperature that algae can survive at?

Based on the habitat of Algaes, a classification called "Thermophytes" can bear high temperature. The Thermophyte algaes use to grow around hot springs and can live around 70°C.

Please find below the reference for all classifications and more details.

http://www.yourarticlelibrary.com/biology/8-types-of-algae-classified-according-to-their-habitats/7098/

http://www.biologydiscussion.com/essay/essay-on-algae/20891


What determines the amount of data you would get from a sequencing experiment?

On an Illumina machine, the instrument runs as many cycles as you tell it to.  If you tell it to run 150 cycles, you will get 150-mers as output.


Why is there Turner syndrome if one of the X chrosomes is inactivated anyway?

Pseudoautosomal region in mammals

On sexual chromosomes, we have a so-called PseudoAutosomal Region (PAR). The PAR is the region which still recombine with the Y chromosome (in males only) and is though to be important to allow separation of chromosomes during meiosis.

Pseudoautosomal region and dosage compensation

Because the PAR is diploid in males too, there is no need for a mechanism of dosage compensation and hence, in females, the PAR of the inactivated X-chromosome remain active.

Turner Syndrome

Turner syndrome is caused by an issue of dosage of functional elements found in the PAR. In people having Turner syndrome the PAR is haploid, while it remains diploid in both healthy males and healthy females.

Here is a small review paragraph from Sybert and McCauley (2004) that report the evidences suggesting that Down syndrome is caused by haploidy in the PAR. Please see the linked paper directly for further references.

  Loss of interstitial or terminal long-arm material of the X chromosome (Xq) can result in short stature and primary or secondary ovarian failure.15 Deletions distal to Xq21 appear to have no effect on stature. In general, loss of the short arm (Xp) results in the full phenotype. Very distal Xp deletions are compatible with, but do not ensure, normal ovarian function. Loss of this region usually confers short stature and the typical skeletal changes, in part as a result of haploinsufficiency of the short stature–homeobox (SHOX) gene, located in the pseudoautosomal region of Y and Xp. The SHOX gene is probably not the only gene responsible for the skeletal features. Aneuploidy itself may contribute to growth failure. Loss of a region at Xp22.3 appears to be associated with the neurocognitive problems in Turner's syndrome. Loss of the testis-determining factor (SRY) gene locus on the short arm of the Y chromosome (e.g., 46,X,del(Yp)) also leads to the phenotype of Turner's syndrome, even without a 45,X cell population. A region on Xp11.4 has been proposed as critical for the development of lymphedema.